Dermoscopy in General Dermatology for Skin of Color [1 ed.] 0367418401, 9780367418403

Table of contents :
Cover
Half Title
Title
Copyright
Contents
List of contributors
Preface
Introduction
Part I Inflammatory and infiltrative diseases
1. Papulosquamous disorders
1.1 Psoriasis
1.2 Dermatitis
1.3 Lichen planus
1.4 Lichen nitidus
1.5 Pityriasis rosea
1.6 Pityriasis rubra pilaris
1.7 Porokeratosis
1.8 Pityriasis lichenoides
1.9 Lichen striatus
1.10 Lichen simplex chronicus and lichenification
1.11 Frictional lichenoid dermatitis
2. Other papulonodular disorders
2.1 Papular acantholytic dermatoses
2.2 Papular urticaria
2.3 Prurigo nodularis
2.4 Acquired perforating dermatoses
3. Non-infectious granulomatous disorders and connective tissue diseases
3.1 Sarcoidosis
3.2 Necrobiosis lipoidica
3.3 Granuloma annulare
3.4 Lupus miliaris disseminatus faciei
3.5 Lupus erythematosus
3.6 Dermatomyositis
3.7 Morphea and systemic sclerosis
3.8 Lichen sclerosus
4. Facial inflammatory dermatoses
4.1 Acne vulgaris
4.2 Rosacea
4.3 Seborrheic dermatitis
4.4 Pseudofolliculitis
4.5 Granuloma faciale
5. Hyperpigmented dermatoses
5.1 Lichen planus pigmentosus
5.2 Ashy dermatosis
5.3 Dowling-Degos disease
5.4 Macular amyloidosis and lichen amyloidosis
5.5 Friction melanosis
5.6 Terra firma-forme dermatosis
5.7 Dermatosis neglecta
5.8 Melasma
5.9 Exogenous ochronosis
5.10 Riehl melanosis (pigmented contact dermatitis)
5.11 Erythema ab igne
5.12 Pigmentary demarcation lines
5.13 Acanthosis nigricans
5.14 Post-inflammatory hyperpigmentation
5.15 Seborrheic melanosis
5.16 Gougerot-Carteaud syndrome
5.17 Nevus of Ota and Becker nevus
6. Hypopigmented dermatoses
6.1 Vitiligo
6.2 Idiopathic guttate hypomelanosis
6.3 Progressive macular hypomelanosis
6.4 Post-inflammatory hypopigmentation
6.5 Achromic nevus and hypomelanosis of Ito
6.6 Ash-leaf macules
6.7 Hypopigmented leprosy
6.8 Pityriasis alba
7. Primary cutaneous lymphomas
7.1 Mycosis fungoides
7.2 Other cutaneous lymphomas
8. Miscellaneous
8.1 Hailey-Hailey disease
8.2 Fixed drug eruption
8.3 Mastocytoses
8.4 Fordyce spots
8.5 Striae
8.6 Keratolysis exfoliative
8.7 Nevus comedonicus
8.8 Cutaneous vasculitis
8.9 Pigmented purpuric dermatoses
8.10 Cutaneous xanthomas
8.11 Xanthogranuloma
8.12 Prayer nodules
8.13 Cutaneous mucinoses
8.14 Ichthyosis vulgaris and x-linked ichthyosis
8.15 Granular parakeratosis
Part II Infectious diseases
9. Bacterial infections
9.1 Leprosy
9.2 Cutaneous tuberculosis
9.3 Impetigo and ecthyma simplex
9.4 Bacterial folliculitis
9.5 Corynebacterium-associated dermatoses
10. Parasitoses
10.1 Cutaneous leishmaniasis
10.2 Demodicosis
10.3 Scabies
10.4 Pediculosis
10.5 Cutaneous larva migrans
11. Mycoses
11.1 Tinea corporis
11.2 Tinea capitis
11.3 Pityriasis versicolour
11.4 Tinea nigra
11.5 Mycetoma (Madura foot)
11.6 Sporotrichosis
11.7 Chromoblastomycosis
12. Viral infections
12.1 Common, plane and genital warts
12.2 Molluscum contagiosum
12.3 Hand, Foot and Mouth disease
Part III Hair, nail and mucosal diseases
13. Hair disorders (Trichoscopy)
13.1 Introduction
13.2 Non-scarring alopecias
13.3 Scarring alopecias
14. Nail disorders (Onychoscopy)
14.1 Introduction
14.2 Inflammatory conditions
14.3 Onychomycosis and other infections
14.4 Traumatic disorders
15. Mucosal disorders (Mucoscopy)
15.1 Scaly disorders
15.2 Leukokeratotic disorders
15.3 Erosive/crusting disorders
15.4 Pigmentary inflammatory/infectious disorders
15.5 Miscellaneous
Index

Citation preview

Dermoscopy in General Dermatology for Skin of Colour

Dermoscopy in General Dermatology for Skin of Colour Edited by

Enzo Errichetti, MD, Msc, PhD Institute of Dermatology, Santa Maria della Misericordia University Hospital, Udine, Italy Aimilios Lallas, MD, MSc, PhD First Department of Dermatology, Aristotle University, Thessaloniki, Greece

First edition published 2022 by CRC Press 2 Park Square, Milton Park, Abingdon, Oxon, OX14 4RN and by CRC Press 6000 Broken Sound Parkway NW, Suite 300, Boca Raton, FL 33487–2742 © 2022 Taylor & Francis Group, LLC CRC Press is an imprint of Informa UK Limited This book contains information obtained from authentic and highly regarded sources. While all reasonable efforts have been made to publish reliable data and information, neither the authors nor the publisher can accept any legal responsibility or liability for any errors or omissions that may be made. The publishers wish to make clear that any views or opinions expressed in this book by individual editors, authors or contributors are personal to them and do not necessarily reflect the views/opinions of the publishers. The information or guidance contained in this book is intended for use by medical, scientific or health-care professionals and is provided strictly as a supplement to the medical or other professional’s own judgement, their knowledge of the patient’s medical history, relevant manufacturer’s instructions and the appropriate best practice guidelines. Because of the rapid advances in medical science, any information or advice on dosages, procedures or diagnoses should be independently verified. The reader is strongly urged to consult the relevant national drug formulary and the drug companies’ and device or material manufacturers’ printed instructions, and their websites, before administering or utilizing any of the drugs, devices or materials mentioned in this book. This book does not indicate whether a particular treatment is appropriate or suitable for a particular individual. Ultimately it is the sole responsibility of the medical professional to make his or her own professional judgements, so as to advise and treat patients appropriately. The authors and publishers have also attempted to trace the copyright holders of all material reproduced in this publication and apologize to copyright holders if permission to publish in this form has not been obtained. If any copyright material has not been acknowledged please write and let us know so we may rectify in any future reprint. All rights reserved. No part of this book may be reprinted or reproduced or utilised in any form or by any electronic, mechanical, or other means, now known or hereafter invented, including photocopying and recording, or in any information storage or retrieval system, without permission in writing from the publishers. For permission to photocopy or use material electronically from this work, access www.copyright.com or contact the Copyright Clearance Center, Inc. (CCC), 222 Rosewood Drive, Danvers, MA 01923, 978–750–8400. For works that are not available on CCC please contact [email protected]. uk Trademark notice: Product or corporate names may be trademarks or registered trademarks and are used only for identification and explanation without intent to infringe. British Library Cataloguing-in-Publication Data A catalogue record for this book is available from the British Library Library of Congress Cataloging‑in‑Publication Data Names: Errichetti, Enzo, editor. | Lallas, Aimilios, editor. Title: Dermoscopy in general dermatology for skin of colour / edited by Enzo Errichetti, Aimilios Lallas. Description: First edition. | Boca Raton : CRC Press, 2022. | Includes bibliographical references and index. Identifiers: LCCN 2021011708 (print) | LCCN 2021011709 (ebook) | ISBN 9780367418403 (hbk) | ISBN 9781032068602 (pbk) | ISBN 9780367816483 (ebk) Subjects: MESH: Dermoscopy | Skin Diseases–diagnosis | Skin Pigmentation | Ethnic Groups Classification: LCC RC280.S5 (print) | LCC RC280.S5 (ebook) | NLM WR 141 | DDC 616.5—dc23 LC record available at https://lccn.loc.gov/2021011708 LC ebook record available at https://lccn.loc.gov/2021011709 ISBN: 978-0-367-41840-3 (hbk) ISBN: 978-1-032-06860-2 (pbk) ISBN: 978-0-367-81648-3 (ebk) DOI: 10.1201/9780367816483 Typeset in Times LT Std by Apex CoVantage, LLC

To my wife, Sabrina, and my sons, Mattia and Martina, for giving me the energy to face all the life challenges.

To my patients, the best teachers to learn from.

Enzo Errichetti

To Chrysa, Magda and Zoe, my closest collaborators.

Aimilios Lallas

Contents

Contents

Contents

List of contributors���������������������������������������������������������������������������������������������������������������������������������������������������������������������������xi Preface������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������ xiii Introduction�����������������������������������������������������������������������������������������������������������������������������������������������������������������������������������xv

Part I Inflammatory and infiltrative diseases 1. Papulosquamous disorders�����������������������������������������������������������������������������������������������������������������������������������������������������3 Enzo Errichetti, Balachandra Ankad, Shekhar Neema, Ahmed Sadek, Dalia Hossam, Abhijeet Kumar Jha, Feroze Kaliyadan, Jayasree Puravoor, Soumil Khare and Aimilios Lallas 1.1 Psoriasis�������������������������������������������������������������������������������������������������������������������������������������������������������������������������3 1.2 Dermatitis����������������������������������������������������������������������������������������������������������������������������������������������������������������������7 1.3 Lichen planus��������������������������������������������������������������������������������������������������������������������������������������������������������������� 11 1.4 Lichen nitidus���������������������������������������������������������������������������������������������������������������������������������������������������������������16 1.5 Pityriasis rosea������������������������������������������������������������������������������������������������������������������������������������������������������������� 17 1.6 Pityriasis rubra pilaris��������������������������������������������������������������������������������������������������������������������������������������������������19 1.7 Porokeratosis����������������������������������������������������������������������������������������������������������������������������������������������������������������20 1.8 Pityriasis lichenoides���������������������������������������������������������������������������������������������������������������������������������������������������21 1.9 Lichen striatus��������������������������������������������������������������������������������������������������������������������������������������������������������������23 1.10 Lichen simplex chronicus and lichenification���������������������������������������������������������������������������������������������������������������������������������������������������������������25 1.11 Frictional lichenoid dermatitis�������������������������������������������������������������������������������������������������������������������������������������27 2. Other papulonodular disorders�������������������������������������������������������������������������������������������������������������������������������������������29 Enzo Errichetti, Balachandra Ankad, Bengu Nisa Akay, Richard Usatine and Aimilios Lallas 2.1 Papular acantholytic dermatoses���������������������������������������������������������������������������������������������������������������������������������29 2.2 Papular urticaria���������������������������������������������������������������������������������������������������������������������������������������������������������� 31 2.3 Prurigo nodularis���������������������������������������������������������������������������������������������������������������������������������������������������������32 2.4 Acquired perforating dermatoses��������������������������������������������������������������������������������������������������������������������������������33 3. Non-infectious granulomatous disorders and connective tissue diseases������������������������������������������������������������������������35 Enzo Errichetti, Ahmed Sadek, Balachandra Ankad, Dalia Hossam, Abhijeet Kumar Jha, Shekhar Neema, Vinay Keshavamurthy, Horacio Cabo, Nkechi Enechukwu, Adebola Ogunbiyi, Aimilios Lallas and Payal Chauhan 3.1 Sarcoidosis�������������������������������������������������������������������������������������������������������������������������������������������������������������������35 3.2 Necrobiosis lipoidica���������������������������������������������������������������������������������������������������������������������������������������������������36 3.3 Granuloma annulare����������������������������������������������������������������������������������������������������������������������������������������������������38 3.4 Lupus miliaris disseminatus faciei������������������������������������������������������������������������������������������������������������������������������39 3.5 Lupus erythematosus���������������������������������������������������������������������������������������������������������������������������������������������������39 3.6 Dermatomyositis����������������������������������������������������������������������������������������������������������������������������������������������������������42 3.7 Morphea and systemic sclerosis����������������������������������������������������������������������������������������������������������������������������������45 3.8 Lichen sclerosus�����������������������������������������������������������������������������������������������������������������������������������������������������������47 4. Facial inflammatory dermatoses����������������������������������������������������������������������������������������������������������������������������������������� 51 Enzo Errichetti, Feroze Kaliyadan, Jayasree Puravoor, Balachandra Ankad, Bengu Nisa Akay and Aimilios Lallas 4.1 Acne vulgaris��������������������������������������������������������������������������������������������������������������������������������������������������������������� 51 4.2 Rosacea������������������������������������������������������������������������������������������������������������������������������������������������������������������������52 4.3 Seborrheic dermatitis���������������������������������������������������������������������������������������������������������������������������������������������������53 4.4 Pseudofolliculitis����������������������������������������������������������������������������������������������������������������������������������������������������������53 4.5 Granuloma faciale��������������������������������������������������������������������������������������������������������������������������������������������������������55

viii

Contents

5. Hyperpigmented dermatoses�����������������������������������������������������������������������������������������������������������������������������������������������57 Shekhar Neema 5.1 Lichen planus pigmentosus������������������������������������������������������������������������������������������������������������������������������������������57 5.2 Ashy dermatosis�����������������������������������������������������������������������������������������������������������������������������������������������������������58 5.3 Dowling-Degos disease������������������������������������������������������������������������������������������������������������������������������������������������60 5.4 Macular amyloidosis and lichen amyloidosis�������������������������������������������������������������������������������������������������������������������������������������������������������� 61 5.5 Friction melanosis��������������������������������������������������������������������������������������������������������������������������������������������������������62 5.6 Terra firma-forme dermatosis��������������������������������������������������������������������������������������������������������������������������������������63 5.7 Dermatosis neglecta�����������������������������������������������������������������������������������������������������������������������������������������������������63 5.8 Melasma�����������������������������������������������������������������������������������������������������������������������������������������������������������������������64 5.9 Exogenous ochronosis��������������������������������������������������������������������������������������������������������������������������������������������������65 5.10 Riehl melanosis (pigmented contact dermatitis)����������������������������������������������������������������������������������������������������������66 5.11 Erythema ab igne���������������������������������������������������������������������������������������������������������������������������������������������������������67 5.12 Pigmentary demarcation lines�������������������������������������������������������������������������������������������������������������������������������������67 5.13 Acanthosis nigricans����������������������������������������������������������������������������������������������������������������������������������������������������68 5.14 Post-inflammatory hyperpigmentation������������������������������������������������������������������������������������������������������������������������69 5.15 Seborrheic melanosis���������������������������������������������������������������������������������������������������������������������������������������������������70 5.16 Gougerot-Carteaud syndrome�������������������������������������������������������������������������������������������������������������������������������������71 5.17 Nevus of Ota and Becker nevus�����������������������������������������������������������������������������������������������������������������������������������72 6. Hypopigmented dermatoses�������������������������������������������������������������������������������������������������������������������������������������������������75 Shekhar Neema 6.1 Vitiligo�������������������������������������������������������������������������������������������������������������������������������������������������������������������������75 6.2 Idiopathic guttate hypomelanosis��������������������������������������������������������������������������������������������������������������������������������77 6.3 Progressive macular hypomelanosis����������������������������������������������������������������������������������������������������������������������������77 6.4 Post-inflammatory hypopigmentation�������������������������������������������������������������������������������������������������������������������������79 6.5 Achromic nevus and hypomelanosis of Ito������������������������������������������������������������������������������������������������������������������80 6.6 Ash-leaf macules����������������������������������������������������������������������������������������������������������������������������������������������������������80 6.7 Hypopigmented leprosy�����������������������������������������������������������������������������������������������������������������������������������������������82 6.8 Pityriasis alba���������������������������������������������������������������������������������������������������������������������������������������������������������������82 7. Primary cutaneous lymphomas�������������������������������������������������������������������������������������������������������������������������������������������85 Tomas Huerta and Trilokraj Tejasvi 7.1 Mycosis fungoides�������������������������������������������������������������������������������������������������������������������������������������������������������85 7.2 Other cutaneous lymphomas���������������������������������������������������������������������������������������������������������������������������������������88 8. Miscellaneous�������������������������������������������������������������������������������������������������������������������������������������������������������������������������91 Feroze Kaliyadan, Jayasree Puravoor, Balachandra Ankad, Richard Usatine, Aimilios Lallas, Bengu Nisa Akay, Nirmal Balakrishnan and Enzo Errichetti 8.1 Hailey-Hailey disease��������������������������������������������������������������������������������������������������������������������������������������������������91 8.2 Fixed drug eruption�����������������������������������������������������������������������������������������������������������������������������������������������������92 8.3 Mastocytoses����������������������������������������������������������������������������������������������������������������������������������������������������������������93 8.4 Fordyce spots���������������������������������������������������������������������������������������������������������������������������������������������������������������94 8.5 Striae����������������������������������������������������������������������������������������������������������������������������������������������������������������������������94 8.6 Keratolysis exfoliative��������������������������������������������������������������������������������������������������������������������������������������������������95 8.7 Nevus comedonicus�����������������������������������������������������������������������������������������������������������������������������������������������������96 8.8 Cutaneous vasculitis����������������������������������������������������������������������������������������������������������������������������������������������������97 8.9 Pigmented purpuric dermatoses����������������������������������������������������������������������������������������������������������������������������������97 8.10 Cutaneous xanthomas��������������������������������������������������������������������������������������������������������������������������������������������������99 8.11 Xanthogranuloma������������������������������������������������������������������������������������������������������������������������������������������������������100 8.12 Prayer nodules������������������������������������������������������������������������������������������������������������������������������������������������������������102 8.13 Cutaneous mucinoses������������������������������������������������������������������������������������������������������������������������������������������������103 8.14 Ichthyosis vulgaris and x-linked ichthyosis�����������������������������������������������������������������������������������������������������������������������������������������������������105 8.15 Granular parakeratosis�����������������������������������������������������������������������������������������������������������������������������������������������106

Contents

ix

Part II Infectious diseases 9. Bacterial infections�������������������������������������������������������������������������������������������������������������������������������������������������������������� 111 Balachandra Ankad, Vinay Keshavamurthy, Shekhar Neema, Payal Chauhan and Enzo Errichetti 9.1 Leprosy���������������������������������������������������������������������������������������������������������������������������������������������������������������������� 111 9.2 Cutaneous tuberculosis���������������������������������������������������������������������������������������������������������������������������������������������� 115 9.3 Impetigo and ecthyma simplex���������������������������������������������������������������������������������������������������������������������������������� 117 9.4 Bacterial folliculitis��������������������������������������������������������������������������������������������������������������������������������������������������� 119 9.5 Corynebacterium-associated dermatoses������������������������������������������������������������������������������������������������������������������120 10. Parasitoses���������������������������������������������������������������������������������������������������������������������������������������������������������������������������� 121 Enzo Errichetti, Ahmed Sadek, Dalia Hossam, Abhijeet Kumar Jha, Aimilios Lallas and Bengu Nisa Akay 10.1 Cutaneous leishmaniasis�������������������������������������������������������������������������������������������������������������������������������������������� 121 10.2 Demodicosis���������������������������������������������������������������������������������������������������������������������������������������������������������������123 10.3 Scabies�����������������������������������������������������������������������������������������������������������������������������������������������������������������������123 10.4 Pediculosis�����������������������������������������������������������������������������������������������������������������������������������������������������������������125 10.5 Cutaneous larva migrans�������������������������������������������������������������������������������������������������������������������������������������������126 11. Mycoses���������������������������������������������������������������������������������������������������������������������������������������������������������������������������������127 Enzo Errichetti, Balachandra Ankad, Manas Chatterjee, Piergiacomo Calzavara Pinton, Vincenzo Maione and Payal Chauhan 11.1 Tinea corporis������������������������������������������������������������������������������������������������������������������������������������������������������������127 11.2 Tinea capitis���������������������������������������������������������������������������������������������������������������������������������������������������������������129 11.3 Pityriasis versicolour��������������������������������������������������������������������������������������������������������������������������������������������������130 11.4 Tinea nigra�����������������������������������������������������������������������������������������������������������������������������������������������������������������132 11.5 Mycetoma (Madura foot)�������������������������������������������������������������������������������������������������������������������������������������������132 11.6 Sporotrichosis������������������������������������������������������������������������������������������������������������������������������������������������������������ 133 11.7 Chromoblastomycosis������������������������������������������������������������������������������������������������������������������������������������������������ 133 12. Viral infections��������������������������������������������������������������������������������������������������������������������������������������������������������������������137 Feroze Kaliyadan, Jayasree Puravoor, Ahmed Sadek, Dalia Hossam and Enzo Errichetti 12.1 Common, plane and genital warts�����������������������������������������������������������������������������������������������������������������������������137 12.2 Molluscum contagiosum��������������������������������������������������������������������������������������������������������������������������������������������140 12.3 Hand, Foot and Mouth disease���������������������������������������������������������������������������������������������������������������������������������� 141

Part III Hair, nail and mucosal diseases 13. Hair disorders (Trichoscopy)��������������������������������������������������������������������������������������������������������������������������������������������� 145 Nkechi Enechukwu and Adebola Ogunbiyi 13.1 Introduction���������������������������������������������������������������������������������������������������������������������������������������������������������������� 145 13.2 Non-scarring alopecias����������������������������������������������������������������������������������������������������������������������������������������������150 13.3 Scarring alopecias������������������������������������������������������������������������������������������������������������������������������������������������������160 14. Nail disorders (Onychoscopy)��������������������������������������������������������������������������������������������������������������������������������������������� 173 Balachandra Ankad and Balkrishna Nikam 14.1 Introduction���������������������������������������������������������������������������������������������������������������������������������������������������������������� 173 14.2 Inflammatory conditions�������������������������������������������������������������������������������������������������������������������������������������������� 174 14.3 Onychomycosis and other infections������������������������������������������������������������������������������������������������������������������������� 179 14.4 Traumatic disorders��������������������������������������������������������������������������������������������������������������������������������������������������� 186 15. Mucosal disorders (Mucoscopy)���������������������������������������������������������������������������������������������������������������������������������������� 189 Abhijeet Kumar Jha 15.1 Scaly disorders����������������������������������������������������������������������������������������������������������������������������������������������������������� 189 15.2 Leukokeratotic disorders������������������������������������������������������������������������������������������������������������������������������������������� 191 15.3 Erosive/crusting disorders������������������������������������������������������������������������������������������������������������������������������������������194 15.4 Pigmentary inflammatory/infectious disorders���������������������������������������������������������������������������������������������������������196 15.5 Miscellaneous������������������������������������������������������������������������������������������������������������������������������������������������������������198 Index���������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������������201

Contributors

Contributors

Contributors

Balachandra Ankad Department of Dermatology, Venereology and Leprosy SN Medical College Bagalkot, India

Feroze Kaliyadan Faculty of Dermatology, College of Medicine King Faisal University Al Ahsa, Saudi Arabia

Nirmal Balakrishnan Dermal Square Skin Clinic and Meenakshi Mission Hospital Madurai, India

Vinay Keshavamurthy Department of Dermatology, Venereology and Leprology Postgraduate Institute of Medical Education and Research Chandigarh, India

Horacio Cabo Dermatology Department, Instituto de Investigaciones Médicas A. Lanari University of Buenos Aires Buenos Aires, Argentina

Soumil Khare Department of Dermatology All India Institute of Medical Sciences Raipur, India

Piergiacomo Calzavara Pinton Department of Dermatology Spedali Civili, University of Brescia Brescia, Italy

Abhijeet Kumar Jha Department of Dermatology and STD Patna Medical College and Hospital Patna, India

Manas Chatterjee Department of Dermatology Command Hospital (Eastern Command) Kolkata, India

Aimilios Lallas First Department of Dermatology Aristotle University Thessaloniki, Greece

Payal Chauhan Department of Dermatology, Venereology and Leprosy Himalayan Institute of Medical Sciences Swami Rama Himalayan University Dehradun, India

Vincenzo Maione Department of Dermatology Spedali Civili, University of Brescia Brescia, Italy

Nkechi Enechukwu Dermatology Unit, Department of Internal Medicine Nnamdi Azikiwe University Anambra, Nigeria Enzo Errichetti Institute of Dermatology Santa Maria della Misericordia University Hospital Udine, Italy Dalia Hossam Department of Dermatology and STD Patna Medical College & Hospital Patna, India Tomas Huerta Department of Dermatology, University of Michigan Ann Arbor, Michigan, USA

Shekhar Neema Department of Dermatology Armed Forces Medical College Pune, India Balkrishna Nikam Department of Dermatology Krishna Institute of Medical Sciences Karad, India Bengu Nisa Akay Department of Dermatology, Ankara University School of Medicine Ankara, Turkey Adebola Ogunbiyi Department of Medicine, College of Medicine University of Ibadan Oyo, Nigeria

xii Jayasree Puravoor Medical Trust Hospital Cochin, India Ahmed Sadek Department of Dermatology, Venereology and Andrology Al-Azhar University Faculty of Medicine Cairo, Egypt Trilokraj Tejasvi Department of Dermatology University of Michigan Ann Arbor, Michigan, USA

Contributors Richard Usatine Department of Dermatology and Cutaneous Surgery Department of Family and Community Medicine University of Texas Health San Antonio San Antonio, Texas, USA

Preface Dermoscopy has become a key part of the dermatologist’s diagnostic armamentarium as it allows to explore findings not seen with the naked eye. Besides its classic use in assessing pigmented and non-pigmented skin tumours, it is gaining significant appreciation in the field of non-neoplastic diseases as a supportive tool to facilitate the clinical differential diagnosis. The possible application of dermoscopy for non-neoplastic dermatoses, including inflammatory, infectious and infiltrative conditions, increases the possibilities to use this technique also in dark-skinned patients, for which it was classically used less due to the lower incidence of cutaneous neoplastic lesions. However, it does require practitioners to be aware of several points of difference from subjects with lighter phototypes as presentation of dermatological diseases in skin of colour may remarkably differ due to the diverse background of colour and specific histological reaction patterns. Moreover, there are some dermatoses that are exclusively or predominantly seen in darker skin for which dermoscopy may serve as a support for their recognition. In this book, we brought together the experience of international experts to document clinical and dermoscopic patterns of non-tumoural dermatoses in phototypes IV to VI (from subcontinental Asian, North African, South American, to African skin) by providing over 700 illustrations, with the hope of helping clinicians to improve their ability to recognize dermatological diseases when dealing with dark-skinned patients. Enzo and Aimilios

Introduction

Introduction

Dermoscopy for skin of colour

Enzo Errichetti and Aimilios Lallas

0.1  General overview Dermoscopy (or dermatoscopy) is a fascinating bridge between clinical and histological assessment that has become a key part of the dermatologist’s diagnostic armamentarium because of its ability to highlight findings not visible to the naked eye.1–3 Even though it has been classically used in assisting the diagnosis of both pigmented and nonpigmented skin tumours, growing evidence supports that dermoscopy may be of aid even in facilitating the recognition of nonneoplastic dermatoses (“general dermatology”), including inflammatory, infectious and infiltrative disorders, as well as nail and hair diseases, thereby increasing diagnostic accuracy and reducing the number of cases requiring biopsy.1–3 The possible usefulness of dermoscopic examination in the field of nonneoplastic dermatoses and nail/hair disorders has led to an increase in its popularity also in dark-skinned populations (phototypes IV, V and VI), for which it has been classically used less because of the lower incidence of skin tumours.4 However, recent studies have shown that dermoscopic semiology in darker phototypes may be significantly different from Caucasian skin because of the diverse background of colour and specific reaction patterns typical of darker phototypes (e.g., lability of pigment and greater tendency for follicular or sclerotic reactions).4,5 Moreover, there are some dermatoses that are exclusively or predominantly seen in skin of colour for which no data are available from published studies on lighter phototypes.4 To deal with these issues, several studies on such a topic have been published to enrich the knowledge on dermoscopic features of nonneoplastic dermatoses in skin of colour.4 Regardless of skin phototypes, there is, however, a key rule that needs to be followed when assessing nonneoplastic dermatoses by dermoscopy, the so-called “two-step” approach, which consists of using dermoscopic examination as a second step, always preceded by the establishment of a clinical differential diagnosis.1–3 Indeed, unlike tumoral lesions, dermoscopic findings of nonneoplastic dermatoses are often poorly specific, thus being scarcely useful by themselves.1–3 For example, linear vessels may be seen in many inflammatory dermatoses and cannot be considered as a specific finding for a single condition, but their presence comes in handy when the differential diagnosis stands between dermatitis and mycosis fungoides as they are found only in the latter.1–3 Another possible issue in the use of dermoscopy in nontumoural conditions is that features of a specific dermatosis may significantly vary according to the development stage (“age”) of each lesion.1–3 In fact, only well-developed (active) lesions usually display possibly characterizing dermoscopic features, which reflect well-expressed histological changes.1–3 Therefore, the more the lesions assessed the greater the likelihood of observing relevant dermoscopic clues.1–3

0.2 Selection of the optimal equipment for non-tumoral dermatoses Whereas pigmentary structures and vessels are the main dermoscopic findings to evaluate when using dermoscopy in the assessment of skin tumours, nontumoural dermatoses are often typified by a complex and variable histological background that is responsible for the presence of several dermoscopic features, with scaling, vessels and follicular findings being the most common ones.1–3 Consequently, it is of utmost importance to select optimal equipment that enhances their visualization. In this regard, it is generally advised to use noncontact polarized dermoscopy as it avoids pressure and does not require a fluid interface, with optimal examination and preservation of vessels and scales.1–3 However, it is possible to come across conditions characterized by a significant hyperkeratosis/scaling that may mask the underlying vascular, pigmentary and follicular structures for which the use of a fluid interface (e.g., oil or ultrasound gel) and direct contact with the skin are needed to complete the dermoscopic assessment.1–3

0.3 Basic dermoscopic parameters to evaluate in general dermatology In general, each non-tumoral condition is characterized by one or two predominant criteria on dermoscopy, which are defined as structures seen in the larger part of the lesion prevailing over other coexisting features.1,6 Although a well-established and structured approach for the analysis of dermoscopic images is available in the field of tumoral diseases, the criteria and terminology used for inflammatory dermatoses in the literature are often variable, metaphoric and poorly comprehensible, with consequent lack of a systematic analytic approach.1,6 For this reason, a set of five dermoscopic parameters (with several subitems) has been proposed by a consensus document of the International Dermoscopy Society as a basic guide to use in general dermatology.6 This has been subsequently validated for the use in skin of colour:7

0.3.1 Vessels 0.3.1.1  Vessels morphology • Dotted vessels (Figure 0.1A). This category includes roundish vessels of any size, without discriminating dotting from pinpoint or globular vessels, which anyhow differ only in the diameter. Quite frequently, dotted vessels of different diameters are simultaneously present in the same lesion. Dotted vessels can be seen in the majority of the common inflammatory

xvi

Introduction

A

B

A

C

D

C

FIGURE 0.1  Morphologic types of vessels: dotted vessels of variable diameter (A), linear vessels not curved and without branches (B), linear vessels with branches (C), and linear curved vessels (D).

skin diseases. They were initially described as the dermoscopic hallmark of psoriasis, but later it was shown that many other inflammatory dermatoses dermoscopically display dotted vessels, including dermatitis (all types), lichen planus, pityriasis rosea, porokeratosis, etc. • Linear vessels (not curved and without branches) (Figure  0.1B). Linear vessels are very frequently present in sun-damaged skin. They are also seen in lesions of any disease treated with topical steroids for long periods. The most frequent skin disease characterized by linear vessels is rosacea, which is typified by a specific arrangement of the vessels in polygons (polygonal vessels). • Linear vessels with branches (Figure 0.1C). They are somehow similar to the typical vessels seen in basal cell carcinoma. They can be seen in granulomatous skin diseases (sarcoidosis, tuberculosis) and at the late stage of discoid lupus erythematosus. • Linear curved vessels (Figure  0.1D). They are similar to the so-called comma vessels that are frequently seen in dermal nevi. They can be found in lichen planus, granulomatous disorders and also in mycosis fungoides.

B

D

E

FIGURE 0.2  Possible distributions of vessels: uniform (A), peripheral (B), clustered (C), unspecific (D), and reticular (E).

• Unspecific (Figure  0.2D). The vascular structures are arranged randomly without following any specific pattern. It can be seen in many diseases, such as mycosis fungoides and pityriasis rosea. • Reticular (Figure 0.2E). The vascular structures form a kind of network. This arrangement can be seen in psoriasis (dotted vessels) and is also very characteristic of rosacea (linear vessels).

0.3.2 Scales 0.3.2.1  Scales colour • White (Figure 0.3A). This is the most frequent scale colour and can be found in most of the erythematosquamous and papulosquamous skin diseases, such as psoriasis or lichen planus. • Yellow (Figure  0.3B). Yellow crusts are a result of serum extravasation, and yellow scales, a result of serum mixed with keratin. Yellow crusts and scales represent the dermoscopic hallmark of all types of

0.3.1.2  Vessels’ distribution • Uniform (Figure 0.2A). This means that the vascular structures are equally and homogeneously distributed all over the surface of the lesion. This vascular arrangement typifies psoriasis but also lichen simplex chronicus. • Peripheral (Figure  0.2B). Vascular structures are distributed mainly at the peripheral part of the lesion. This arrangement is frequently seen in lichen planus. • Clustered (Figure 0.2C). Vessels are grouped in clusters. It is frequently observed in dermatitis.

A

B

C

FIGURE 0.3  Colour of scales: white scales (A), yellow crusts and scales (B), and brown scales (C).

xvii

Dermoscopy for skin of colour

dermatitis, corresponding histopathologically to the underlying spongiosis. • Brown (Figure  0.3C). Pigmented parakeratosis might occur in several dermatoses and results in the presence of brown-coloured scales. Exogenous pigment represents another possible cause of brown scaling.

0.3.2.2  Scales’ distribution • Diffuse (Figure  0.4A). Scales covering all the surfaces of the lesion. It cannot be considered specific of any diagnosis because diffuse scales can be seen in several hyperkeratotic dermatoses. • Central (Figure 0.4B). Scales accentuated in the centre of the lesion. Again, this scaling pattern cannot be considered as specific as it may be found in more than one conditions, such as psoriasis, discoid lupus erythematosus and hypertrophic lichen planus. • Peripheral (Figure  0.4C). Scales sparing the centre and distributed mainly at the periphery. It is a classic sign of pityriasis rosea but can also be seen in tinea corporis and other entities. • Patchy (Figure  0.4D). Random and a­symmetric distribution of scales. May be seen in several ­ diseases. • Perifollicular (Figure 0.4E). A preferential distribution around hairs is usually observed in conditions characterized by a tropism for follicles, e.g., pityriasis versicolour and seborrheic dermatitis.

0.3.3  Follicular/Eccrine findings 0.3.3.1  Follicular findings • Follicular plugs (Figure  0.5A). Keratin plugs of white or yellow colour filling the follicular openings. It can be found in several diseases but is considered as the dermoscopic hallmark of early-stage discoid lupus erythematosus. • Follicular openings obliteration (Figure  0.5B). Pigmentary obliteration of follicular openings may be found in several facial inflammatory diseases. Although it is not pathognomonic of any specific condition, it is quite common after inflammatory pigmentation because of discoid lupus erythematosus, nevus of Ota and exogenous ochronosis. • Perifollicular white colour (Figure  0.5C). A  whitecoloured circle surrounding each hair follicle and/ or white colour filling the space between follicles. It might correspond to perifollicular fibrosis (e.g., discoid lupus erythematosus), to epidermal hyperplasia (e.g., hypertrophic lichen planus), or to perifollicular depigmentation (e.g., vitiligo). • Perifollicular pigmentation (Figure  0.5D). Pigment accentuated around the hair follicles. It can be seen in some alopecias but also represents the first sign of repigmentation in vitiligo.

0.3.3.2  Eccrine findings • Broken hairs (Figure  0.6A). They may be found in some conditions targeting the follicles, such as tinea corporis, but also as a result of scratching in itchy dermatoses (e.g., eczematous dermatitis and psoriasis). • Perieccrine pigmentation (Figure 0.6B). Such a finding is mainly seen in hypopigmented dermatoses as a result of sparing of the pigment around the eccrine ostia; it is mainly seen in idiopathic guttate hypomelanosis and pityriasis alba. • Eccrine ostia obliteration (Figure  0.6C). This feature is typically observed in pigmentary disorders, especially those involving the face. Some examples include nevus of Ota and exogenous ochronosis.

0.3.4  Other structures The term “other structures” encompasses findings other than vessels, scales and follicular/eccrine features. They represent a result of various histopathologic alterations including epidermal changes, cellular infiltrations, or deposits of melanin or other substances. These structures can be classified according to their colour and morphology as described in the following sections.

0.3.4.1  Other structures – colour • White, which histopathologically might correspond to fibrosis, reduction of melanocytes or melanin, epidermal hyperplasia (acanthosis, hypergranulosis), or calcium deposits. • Brown, corresponding to the presence of melanin in the basal layer of the epidermis or the superficial dermis. • Grey, corresponding to the presence of melanin or ochronotic pigment in the papillary dermis. • Blue, resulting from pigment deposits in the reticular dermis.

A

C

B

D

E

FIGURE 0.4  Possible distributions of scales: diffuse (A), central (B), peripheral (C), patchy (D), and perifollicular (E).

xviii

Introduction

A

B

C

D

FIGURE 0.5  Follicular/eccrine criteria: follicular plugs (A), follicular openings obliteration (B), perifollicular white colour (C), and perifollicular pigmentation (D).

A

B

C

D

FIGURE 0.7  Other structures  – shape: structureless areas focal (A), dots (B), lines (C) and circles (D).

• Orange, which histopathologically corresponds to the presence of dermal granulomas, dense cellular infiltrations, or hemosiderin deposits in the dermis. • Yellow, usually resulting from lipid deposits in the dermis. • Purple, corresponding to extravasation of erythrocytes (purpura).

0.3.4.2  Other structures – morphology • Structureless areas (Figure  0.7A). They might be diffuse, resulting in a relatively homogeneous background. Alternatively, they might be focal, coloured zones of unspecific shape, lacking any recognizable structure. • Dots or globules (Figure 0.7B). • Lines (Figure 0.7C). which might be parallel, reticular, perpendicular, angulated, or non-specifically arranged • Circles (Figure 0.7D).

A

B

C

FIGURE 0.8  Examples of specific clues: Wickham striae of lichen planus (A), peripheral keratotic rim of porokeratosis (B) and “jet with contrail” in scabies (C).

0.3.5  Specific clues A specific clue is considered a feature that, when present, is very strongly suggestive of only one diagnosis. Therefore, specific clues are features that can be seen in only one disease and not in any other entity, especially in those included in the differential diagnosis. Specific clues have been suggested for several diseases, but only a few have been investigated in appropriately designed studies that included control groups. Examples of specific clues are the white crossing lines of lichen planus (Wickham striae), peripheral keratotic rim of porokeratosis and “jet with contrail” seen in scabies (Figure 0.8).

REFERENCES

A

B

C

FIGURE 0.6  Follicular/eccrine criteria: broken hairs (A), perieccrine pigmentation (B) and eccrine ostia obliteration (C).

1. Lallas A, Errichetti E. Introduction. In: Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press, 2018:xi–xix. 2. Errichetti E, Stinco G. Dermoscopy in general dermatology: A  practical overview. Dermatol Ther (Heidelb) 2016;6:471–507. 3. Errichetti E. Dermoscopy of inflammatory dermatoses (inflammoscopy): An up-to-date overview. Dermatol Pract Concept 2019;9:169–80.

xix

Dermoscopy for skin of colour 4. Errichetti E, Ankad BS, Sonthalia S, et  al. Dermoscopy in general dermatology (non-neoplastic dermatoses) in skin of  colour: A  comparative retrospective study by the International Dermoscopy Society. Eur J Dermatol 2020;30: 688–98. 5. Errichetti E. Dermoscopy of common papulosquamous dermatoses varies between dark (III and IV) and very dark (V and VI) skin phototypes. Dermatol Ther 2021. doi: 10.1111/ dth.14757.





6. Errichetti E, Zalaudek I, Kittler H, et al. Standardization of dermoscopic terminology and basic dermoscopic parameters to evaluate in general dermatology (non-neoplastic dermatoses): An expert consensus on behalf of the International Dermoscopy Society. Br J Dermatol 2020;182:454–67. 7. Errichetti E, Ankad BS, Jha A, et al. International Dermoscopy Society criteria for non-neoplastic dermatoses (general dermatology): validation for skin of colour through a Delphi expert consensus. Int J Dermatol 2021. doi: 10.1111/ijd.15729.

Part I

Inflammatory and Infiltrative Diseases

1 Papulosquamous disorders

Papulosquamous disorders

Dermoscopy for skin of colour

Enzo Errichetti, Balachandra Ankad, Shekhar Neema, Ahmed Sadek, Dalia Hossam, Abhijeet Kumar Jha, Feroze Kaliyadan, Jayasree Puravoor, Soumil Khare and Aimilios Lallas

1.1 Psoriasis 1.1.1 Introduction Psoriasis is a chronic immune-mediated, inflammatory disease mainly involving the skin, nails and joints pathogenetically related to both genetic and environmental factors.1,2 Cutaneous psoriasis is typically considered as a hyperproliferative disorder with an increased proliferation of keratinocytes resulting from a cascade of immunologic reactions driven by several cytokines.1,2 The prevalence rate among dark-skinned populations varies according to the countries, yet it is generally lower than that of Caucasians.1,2 Although psoriasis can manifest at any age, it generally presents two peaks of onset (20–30 and 50–60 years of age).1,2

1.1.2  Clinical presentation Several clinical variants of skin psoriasis do exist, with the most common one being plaque-type psoriasis (also known as psoriasis vulgaris).1,2 This form typically presents with relatively symmetric, well-defined, brownish, violaceous or greyish plaques covered with silvery scales more commonly affecting the scalp, elbows, knees, trunk, genitalia and presacral and palmo-plantar areas (Figures  1.1A–1.6A).1,2 Pruritus may be present, especially in lesions of the scalp.1,2 Residual dyspigmentations (hyper- or hypopigmentations) after the lesions heal are quite common in skin of colour (Figures 1.7A and 1.8A).1,2 Other common forms of psoriasis include guttate psoriasis (acute onset of multiple small scaly papules often triggered by a streptococcal pharyngitis), erythrodermic psoriasis (generalized erythema and scaling affecting >90% of the body surface), genital psoriasis (Figure 1.9A), palmo-plantar or diffuse pustular psoriasis (groups of pinpoint sterile pustules with or without plaques) and inverse psoriasis (well-demarcated plaques with no visible scaling involving the skin folds).1,2 Follicular psoriasis (Figure 1.10A), psoriasis ostracea, psoriasis rupioides (Figure 1.11A), psoriasis figurata, psoriasis gyrata and annular psoriasis are examples of rare variants.1,2 Finally, nail psoriasis is quite common (30%–50% of psoriatic patients) and may manifest with several ungual changes, such as nail pitting, crumbling, Beau lines and mottled lunula in case of matrix involvement and onycholysis, salmon patches, subungual hyperkeratosis and splinter haemorrhages in case of bed involvement.1,2

1.1.3 Dermoscopy The dermoscopic hallmarks of psoriasis are represented by diffuse white scales and uniform dotted vessels (Figure 1.1B), histologically corresponding to hyperkeratosis and tips of dilated vessels in regularly elongated dermal papillae (papillomatosis), respectively.3–5 Notably, even though the prevalence of vascular structures in dark-skinned patients is lower than that in fair-skinned subjects, psoriasis is one the few papulosquamous dermatoses in which vessels are commonly seen on dermoscopy (60%–75% of cases).6,7,8 This is because of the fact that the significant epidermal acanthosis typical of psoriasis makes the skin background lighter, thus enhancing the optical contrast with vessels (Figures 1.1B and 1.2B).6 In hyperkeratotic plaques, thick scales may cover the underlying vascular structures, yet removal of the scales may bring to light the typical vascular pattern.3–6 However, analysis of the scaling pattern (colour and distribution) still remains the main dermoscopic clue in a significant proportion of dark-skinned patients, especially in areas having a thick skin (i.e., scalp or palmo-plantar areas) (Figures 1.3B–1.5B).6 Additionally, vessels are difficult to see also in initial/thin lesions as they are characterized by a limited papillomatosis on histology.3–6 Pigmentary structures (especially focal or diffuse brown structureless areas resulting from basal layer hyperpigmentation) are also not uncommonly seen in psoriasis in ethnic skin (Figure 1.1B).6,7 Further dermoscopic findings of psoriasis include focal structureless white areas (related to epidermal acanthosis) (Figure 1.1B) as well as haemorrhagic dots/areas, erosions and broken hairs resulting from scratching (Figure  1.6B), especially on the scalp and legs.3–6 Additionally, dermoscopy can also help the clinician diagnose psoriasis retrospectively as the typical vascular pattern may also be observed in hypopigmented postinflammatory patches (Figures 1.7B and 1.8B).3–5,8 The dermoscopic pattern of specific subtypes of psoriasis do not significantly differ from each other, except for the scaling amount.3–5,8 Indeed, inverse psoriasis and psoriatic balanitis (Figure 1.9B) classically do not feature scales, whereas scalp and palmo-plantar psoriasis usually reveal a thick hyperkeratotic surface (Figure  1.4B).3–5,8 Nevertheless, there are some clinical forms of psoriasis, which are not so uncommon in dark skin, that may show peculiar dermoscopic findings, such as follicular psoriasis, characterized by irregularly distributed follicular plugs associated with white scaling (Figure  1.10B) and rupioid psoriasis, which displays cone-shaped thick scales (Figure 1.11B).8 DOI: 10.1201/9780367816483-1

4 A

Papulosquamous disorders B

FIGURE 1.1  Plaque-type psoriasis in an Indian woman (A). Dermoscopy reveals diffuse white scales and uniform dotted vessels (better visible in the inset); hypo- and hyperpigmented focal structureless areas are also seen (B).

A

B

FIGURE 1.2  Palmar psoriasis in an Indian man (A). Dermoscopic examination shows uniform dotted vessels over the skin ridges (B).

A

B

FIGURE 1.3  Plaque-type psoriasis of the forehead in an African woman (A), which features only diffuse white scales over a brownish background on dermoscopy (B).

5

Dermoscopy for skin of colour A

B

FIGURE 1.4  Plantar psoriasis in an African man (A). Dermoscopy displays only diffuse white scales with no evident vessel (B).

A

B

FIGURE 1.5  Plaque-type psoriasis involving the knee in an African man (A). Dermoscopic assessment reveals diffuse white scales over a brownish background (B).

A

B

FIGURE 1.6  Scratched psoriatic lesions in an African girl (A). Haemorrhagic dots/areas, erosions and focal white structureless areas are evident on dermoscopy (B).

6

Papulosquamous disorders A

B

FIGURE 1.7  Postinflammatory hypopigmented patches of the face in an Indian psoriatic patient (A). Uniform dotted vessels over a white background are seen on dermoscopic examination (B).

A

B

FIGURE 1.8  Postinflammatory hypopigmented patches of the leg in an Indian psoriatic patient (A) which show uniform dotted vessels over a white background on dermoscopy (B).

A

B

FIGURE 1.9  Psoriatic balanitis in an Indian patient (A). Dermoscopic examination reveals uniform dotted vessels (better visible in the inset) (B).

7

Dermoscopy for skin of colour A

B

FIGURE 1.10  Follicular psoriasis in an Indian man (A). White follicular plugs are seen on dermoscopy (B).

A

B

FIGURE 1.11  Rupioid psoriasis in an Indian man with cone-shaped hyperkeratotic papules and plaques (A). Dermoscopy shows thick concentric scales obscuring the underlying vascular pattern (B). (From Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press.)

1.2 Dermatitis 1.2.1 Introduction The term “dermatitis” (syn. eczema) refers to a group of conditions with different etiopathogenesis that share a similar histological background (i.e., spongiosis) and clinical presentation (itchy eczematous lesions).8–10 The most common forms of dermatitis in skin of colour include allergic contact dermatitis and atopic dermatitis, with the latter representing one of the most frequent reasons for referral to a dermatologist in dark-skinned populations.8–10

1.2.2  Clinical presentation The clinical morphology of eczematous dermatitis varies according to the disease stage.8–10 In detail,

erythematous-oedematous patches, with or without overlying pinpoint vesicles and/or serous drainage, are typically seen in the acute phases (Figure 1.12A), whereas the subacute and chronic stages are respectively characterized by erythematous/brownish-crusted and brownish/greyish lichenified patches (Figures 1.13A–1.15A).8–10 Notably, erythema in dermatitis may be difficult to see in darker phototypes and superficial changes, such as crusting and scaling, may sometimes be the only clinical diagnostic clues (Figures 1.12A and 1.13A).8–10 The lesions localization varies according to the type of dermatitis.8–10 In allergic contact dermatitis, the lesions distribution is affected by the area of contact with the hapten, whereas atopic dermatitis involves the face and extensor extremities in infants and hands (Figure  1.16A) and flexures in children and adults.8–10 Nummular eczema (roundish eczematous lesions) (Figure  1.17A), papular eczema

8 (Figure 1.18A) and follicular eczema (Figure 1.19A) are variants of atopic dermatitis, with the last two forms being quite common in dark skin.8–10

1.2.3 Dermoscopy The dermoscopic features of dermatitis vary according to the evolution stage of the disease.3–6,8 The main dermoscopic feature in acute and subacute phases consists of patchy yellow scales/crusts due to hyperkeratosis and spongiosis/serum exudation (Figures  1.12B–1.15B).3–6,8 Importantly, acute and subacute eczematous lesions in ethnic skin often also reveal patchy brownish scales/crusts as a result of hyperkeratosis, spongiosis and melanin exfoliation, whereas clustered dotted vessels, frequently seen in Caucasian patients, are observed less commonly in darker phototypes (Figures  1.12B–1.17B).3–6,8 Interestingly, sometimes, the only sign of serum exudation is represented by the presence of adherent fabric fibres (Figure  1.15B).3–6,8 Spongiotic vesicles (appearing as browngrey globules) may be seen on palmo-plantar areas as the thicker epidermis typical of such districts makes them less prone to break (Figure 1.16B).3–6,8 Additional features of subacute phases in dark skin include patchy (and less commonly diffuse) white scales, perifollicular scaling, focal structureless white areas (corresponding to epidermal acanthosis), pigmentary findings (e.g., focal structureless brown/grey areas because of basal layer pigmentation and brown dots because of pigment incontinence)

A

Papulosquamous disorders and haemorrhagic areas/dots (resulting from scratching) (Figures 1.12B–1.17B).3–6,8 Chronic lichenified eczematous lesions typically show diffuse white scaling because of hyperkeratosis and patchy or diffuse dotted vessels surrounded by a white halo resulting from dermal papillae vessels dilation and epidermal acanthosis.3–6,8 Patchy yellow/brown scales/crusts are sometimes visible.3–6,8 Further dermoscopic findings include features resulting from scratching (i.e., haemorrhagic areas/dots and crusts, broken hair and superficial erosions), pigmentary structures (focal structureless brown/grey areas and brown dots), follicular plugs (representing follicular hyperkeratosis) and white structureless areas (corresponding to epidermal acanthosis and fibrosis) – for other details see Section  1.10 (Lichen simplex chronicus and lichenification). 3–6,8 Papular eczema usually features roundish white areas with peripheral striae (similar to what is seen in prurigo nodularis – “white starburst” pattern), often with a central yellow crust (Figure 1.18B).3–6,8 Finally, follicular eczema displays a repetitive pattern, namely regularly distributed follicular plugs because of follicular hyperkeratosis surrounded by a white halo because of epidermal acanthosis (Figure 1.19B).3–6,8 Such a pattern is different from that seen in keratosis pilaris (commonly associated to atopic dermatitis), in which it is possible to see follicular scaling and coiled hairs, and disseminate and recurrent infundibulofolliculitis, typically displaying linearly arranged, ill-defined or sharp, white perifollicular areas without follicular plugs (Figure 1.20).3–6,8

B

FIGURE 1.12  Eczematous dermatitis of the dorsum of the right hand in an atopic African girl (A). Dermoscopy patchy yellow/brown scales/crusts, small erosions and clustered dotted haemorrhagic spots resulting from scratching (B). (From Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press.)

9

Dermoscopy for skin of colour A

B

FIGURE 1.13  Atopic dermatitis of the neck in an African boy (A). Dermoscopy reveals patchy brown scales/crusts along with sparse reddish haemorrhagic crusts (B). (Panel B from Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press.)

A

B

FIGURE 1.14  Subacute eczematous lesion of the leg in an atopic Dominican girl (A). Patchy yellow/brown scales/crusts along with multifocal white structureless areas and broken hairs resulting from continuous scratching (B).

A

B

FIGURE 1.15  Allergic contact dermatitis of the abdomen in an African boy (A). Dermoscopic assessment displays patchy yellow/brown scales/crusts along with white lines/structureless areas and adherent fabric fibres (black arrowhead) (B).

10

Papulosquamous disorders A

B

FIGURE 1.16  Palmar eczematous dermatitis in an Indian man (A). Patchy brown scales/crusts, clustered dotted vessels and round brown-grey globules corresponding to spongiotic vesicles are evident on dermoscopy (B).

A

B

FIGURE 1.17  Nummular eczema of the leg in an African woman (A). Dermoscopic examination reveals diffuse white scaling along with sparse brown scales and brown dots/focal structureless areas (B).

A

B

FIGURE 1.18  Papular eczema in an atopic African boy (A). Central yellow crust with peripheral white projections (“white starburst” pattern) is visible on dermoscopy (magnification in the inset) (B).

11

Dermoscopy for skin of colour A

B

FIGURE 1.19  Follicular eczema of the back of an African boy (A). Dermoscopic examination displays regularly spaced follicular plugs with white halos (B).

A

B

FIGURE 1.20  Recurrent infundibulofolliculitis of the back in an African boy (A) typically displaying linearly-arranged, irregular, white perifollicular areas without follicular plugs (B).

1.3  Lichen planus 1.3.1 Introduction Lichen planus (LP) is an inflammatory mucocutaneous disorder more commonly occurring in middle-aged adults and affecting the skin, mucosae and/or nail that is supposed to be related to an autoimmune response to altered self-antigens on basal keratinocytes.8,11,12 No significant racial predisposition has been reported and the incidence in skin of colour is variable, with rates varying from 0.29% in African Americans to 0.1–1% in East Indians.8,11,12

1.3.2  Clinical presentation Several clinical variants of LP of the skin do exist, with classic, hypertrophic and actinic forms being the most common ones in ethnic skin.8,11,12

Classic LP (Figures  1.21A and 1.22A) presents with itchy polygonal, flat-topped, violaceous, brownish, greyish or blackish papules sometimes coalescing into plaques that most commonly involve the flexor surfaces of the wrists and forearms, the dorsal aspects of the hands and the anterior surface of the legs.8,11,12 Post-healing residual hyperpigmented macules/ patches are frequent in dark skin (Figure  1.22A).8,11,12 Oral involvement (Figures  1.23A and 1.24A), with either white (often reticular) plaques or erosions, and penis involvement (Figure 1.25A) are quite common.8,11,12 Hypertrophic LP (Figure  1.27A) manifests as very itchy, thick, brownish plaques with a greyish hyperkeratotic surface that typically involve the anterior shins.8,11,12 Actinic LP (LP actinicus) (Figure  1.28A) is typified by annular hyperpigmented plaques with a violaceous border affecting sunexposed areas (especially the face); several more uncommon morphological variants of actinic LP have been reported, including melasma-like patches, dyschromic papules and classic lichenoid papules.8,11,12

12 Other less common forms of LP include bullous LP (Figure  1.29A), follicular LP (Figure  1.30A), LP pemphigoides, blaschkolinear LP, annular LP, atrophic LP, ulcerative LP and LP-lupus erythematosus overlap syndrome. LP pigmentosus and LP of the scalp and nails are quite common and are described in other chapters of this book.8,11,12

1.3.3 Dermoscopy The dermoscopic hallmark of active lesions of classic LP is represented by the so-called Wickham striae, which are histologically related to hypergranulosis.3–8 They consist of intersecting crossing white lines forming a sort of network (Figure  1.21B), although other morphologies may sometimes be seen, including linear, annular (Figure  1.22B), round, “leaf venation”-like (mimicking the crystal structure of snow) and “starry sky”-like (clustered, follicular white dots).3–8 Wickham striae are also the main dermoscopic clue of mucosal lesions (Figures  1.23B–1.25B).3–8 Notably, the colour of Wickham striae is often bluish-white in darker phototypes (Figures 1.21B, 1.22B and 1.25B).3–8 Unlike Caucasian patients, vessels (peripheral dotted and/or linear vessels) are

A

Papulosquamous disorders seen only in a minority of cases in dark-skinned patients, whereas pigmentary structures (i.e., structureless brown areas resulting from basal layer hyperpigmentation and brown/grey dots related to dermal melanophages/melanin incontinence) are quite frequent (Figure  1.21B) and are the predominant or the sole feature in healing and postinflammatory lesions of classic LP (Figure  1.26).3–8 Additional dermoscopic findings include patchy or central white scaling and purple dots or areas.3–8 In hypertrophic LP, dermoscopy shows follicular plugs (Figure  1.27B) corresponding to follicular hyperkeratosis on histology.3–8 In this variant, Wickham striae are usually absent because they are covered by the overlying hyperkeratosis, whereas they are generally evident in both LP actinicus and bullous LP and present as a peripheral whitish halo in the former (Figure 1.28B) and reticular whitish areas along with crusts (ruptured blisters) in the latter (Figure  1.29B).3–8 Additionally, LP actinicus also displays a brown centre (histologically corresponding to pigment incontinence in the dermis) and, sometimes, keratotic follicular plugs (resulting from follicular hyperkeratosis).3–8 This last finding is also typical of follicular LP (Figure 1.30B).3–8

B

FIGURE 1.21  Classic lichen planus of the trunk in an African girl (A). Dermoscopy reveals the typical Wickham striae, presenting as bluish lines arranged in a network, surrounded by grey-brownish dots/structureless areas and no vessel (B). (Panel B from Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press.)

13

Dermoscopy for skin of colour A

B

FIGURE 1.22  Eruptive lichen planus of the back in an African man (A). Dermoscopic examination shows Wickham striae appearing as annular greylight blue structures with a central brown area (B).

A

B

FIGURE 1.23  Lichen planus involving the lips in an Indian man (A). White reticular streaks, red erosions and peripheral linear vessels are seen on dermoscopy (B). (Panel B from Dermatol Pract Concept 2020;10:e2020076.)

A

B

FIGURE 1.24  Lichen planus of the tongue in an Indian man (A). Dermoscopic assessment shows multifocal white structureless areas, red erosions and sparse dotted vessels.

14

Papulosquamous disorders A

B

FIGURE 1.25  Lichen planus affecting the penis in an Indian man (A). Multifocal white structureless areas, corresponding to the Wickham striae, along with patchy grey-bluish structureless areas are evident on dermoscopy (B).

A

B

FIGURE 1.26  Dermoscopy of a healing lesion of lichen planus in a patient with very dark skin: diffuse brownish background is predominant, although remnants of Wickham striae are still evident in the centre (A). Dermoscopy of a healed lesion of lichen planus in a patient with very dark skin: diffuse dark brown pigmentation (B). (From Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press.)

A

B

FIGURE 1.27  Hypertrophic lichen planus of the dorsum of the feet in an Indian patient (A). The main dermoscopic feature is represented by follicular plugs; white scales are also seen (B).

15

Dermoscopy for skin of colour A

B

FIGURE 1.28  Lichen planus actinicus in an Indian man (A). Dermoscopy reveals a central brown pigmentation along with brownish follicular plugs as well as a peripheral whitish-bluish rim (Wickham striae) (arrow) (B). (From Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press.)

A

B

FIGURE 1.29  Bullous lichen planus in an African man (A). In this variant, Wickham striae are often reticular; crusts are typically seen (B). (From Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press.)

A

B

FIGURE 1.30  Follicular lichen planus in an Indian man (A). Thick follicular plugs are visible on dermoscopy; a rainbow-like structure is also seen in the centre of the image (B).

16

1.4  Lichen nitidus 1.4.1 Introduction Lichen nitidus (LN) is an idiopathic inflammatory dermatosis typically characterized by spontaneous resolution in a few years that has been speculated to be induced by allergens causing epidermal and dermal antigen-presenting cells to activate a cell-mediated response.8,12–14 Although it seems to affect blacks more than whites, several studies do not show any racial predilection.8,12–14

1.4.2  Clinical presentation LN in dark-skinned patients presents as pinpoint, hypopigmented, asymptomatic, shiny papules mainly involving the abdomen, chest, extremities and genitalia (especially in men) (Figure  1.31A).8,12–14 Involvement of the mucous membranes, nails, face, palms and soles is possible but uncommon.8,12–14 A variant affecting sun-exposed areas (LN actinicus) has been A

Papulosquamous disorders reported in dark skin (Figure  1.32A).8,12–14 Köbner phenomenon resulting in lesions arranged in a linear pattern is not uncommonly seen in LN.8,12–14

1.4.3 Dermoscopy The dermoscopic hallmark of LN is represented by roundish, homogeneous, whitish areas (one for each papule) typically featuring sharply demarcated margins and a lack of physiological skin markings (Figures 1.31B and 1.32B).6,8,15,16 Such areas are related to the dense lymphohistiocytic inflammatory cell infiltrate that is located in close proximity to the thinned epidermis and enveloped by bordering elongated rete ridges (“claw clutching a ball” appearance), whereas the lack of physiological skin markings would be because of the epidermal-dermal junction flattening (resulting from the pressure by the underlying dermal inflammatory cell infiltrate).6,8,15,16 Dermoscopy may also be helpful in highlighting a possible clinically unnoticeable linear arrangement of some lesions (“micro Köbner phenomenon”) (Figure 1.32B).6,8,15,16 B

FIGURE 1.31  Lichen nitidus of the abdomen of an African boy (A). Dermoscopy reveals well-defined white globules devoid of physiological skin markings (B).

A

B

FIGURE 1.32  Lichen nitidus of the back of the right hand/forearm in an African man (A). The “micro Köbner phenomenon” (linearly arranged and confluent papules) is evident on dermoscopic examination (B).

17

Dermoscopy for skin of colour

groin and lower abdomen) are not uncommon in dark-skinned patients.8,17,18

1.5  Pityriasis rosea 1.5.1 Introduction Pityriasis rosea (PR) is a frequent, self-healing inflammatory skin disease typically occurring in adolescents and young adults without sex or racial predilection that spontaneously heals in 6–10 weeks.8,17,18 Although its etiopathogenesis is not completely known, a possible association with herpes viruses types 6/7 has been proposed.8,17,18

1.5.2  Clinical presentation Typically, the disease initially manifests with a single herald or mother lesion consisting of an oval brownish or grey patch with a scaling collarette having an inner free edge.8,17,18 Such a lesion is followed after a few days by the appearance of multiple asymptomatic or itchy “secondary” lesions that are either oval scaling patches similar to the herald patch or skin-coloured papules (which are sometimes follicular) (Figures 1.33A and 1.34A).8,17,18 Papular variants and postinflammatory hyper- or, less commonly, hypopigmentation are not rare in skin of colour (Figures 1.35A and 1.36A).8,17,18 PR classically affects the proximal extremities and trunk (where the lesions orientation is often parallel to the lines of the cleavage forming a “Christmas tree” distribution).8,17,18 However, involvement of the face and inverse distribution (neck, axilla,

A

1.5.3 Dermoscopy The most characterizing dermoscopic feature of both herald and secondary lesions of PR is a peripheral collarette of scales with a jagged inner free edge, histologically correlating with focal parakeratosis in mounds typical of such a condition (Figure  1.33B).3–8 Notably, such a dermoscopic finding may sometimes be absent, especially in lesions located on the face where lesions tend to display a perifollicular scaling pattern (Figure  1.34B).3–8 Focal or diffuse (as a background) brown structureless areas corresponding to basal layer hyperpigmentation and brown dots because of dermal pigment incontinence are also often seen in PR in dark-skinned patients (Figure 1.33B).3–8 Additional dermoscopic findings of PR in skin of colour include peripheral brown scales (resulting from hyperkeratosis, spongiosis and melanin exfoliation) and focal grey structureless areas (corresponding to basal layer hyperpigmentation and slight acanthosis).3–8 A peculiar dermoscopic feature of papular PR is represented by white structureless areas with ill-defined margins that may be centred around follicles (Figure 1.35B).3–8 Finally, postinflammatory hyperpigmented lesions due to PR usually show structureless brown areas or a brown network (Figure 1.36B).3–8

B

FIGURE 1.33  Pityriasis rosea on the back of an African girl (A). Dermoscopic assessment shows peripheral collarette of scales with a jagged inner free edge and a diffuse brown-grey background (B).

18

Papulosquamous disorders A

B

FIGURE 1.34  Pityriasis rosea on the chest of an African woman (A). Diffuse white scales and perifollicular white scaling along with brown dots are seen on dermoscopy (B).

A

B

FIGURE 1.35  Papular pityriasis rosea on the back of an African man (A). Dermoscopic examination reveals white structureless areas with ill-defined margins (B).

A

B

FIGURE 1.36  Postinflammatory pigmentation due to pityriasis rosea in a Dominican woman (A). Brown network is visible on dermoscopy (B). (Courtesy of Arturo Galvan, MD – Verona, Italy.)

19

Dermoscopy for skin of colour

1.6  Pityriasis rubra pilaris 1.6.1 Introduction Pityriasis rubra pilaris (PRP) is a chronic papulosquamous disorder of unknown aetiology, yet a possible link with some antigenic triggers has been speculated such as streptococcal infections, vaccinations and medications.8,19 It is usually sporadic, but a hereditary form does exist (type V – see Clinical presentation).8,19

1.6.2  Clinical presentation Five forms are typically reported, viz. classical (adult onset [type I] and juvenile onset [type III]), atypical (adult onset [type II] and juvenile onset [type V]) and circumscribed juvenile (type IV).8,19 Classical forms present with follicular hyperkeratotic papules as well as orange-red scaly patches spreading in a cephalocaudal pattern (Figure 1.37A).8,19 A progression to erythroderma, with typical uninvolved skin areas (islands of A

sparing), palmoplantar keratoderma and nail changes are other possible manifestations.8,19 Atypical forms feature follicular hyperkeratosis and either ichthyosiform lesions on the legs along with sparse scalp hair (adult onset) or scleroderma-like change of the hands and feet (juvenile onset).8,19 Circumscribed juvenile PR manifests as scaly erythematous (psoriasis-like) plaques on the elbows and knees (Figure 1.38A), with or without palmoplantar keratoderma.8,19

1.6.3 Dermoscopy The main dermoscopic feature of PRP is represented by follicular scaling/plugs representing follicular hyperkeratosis on histology.6,20,21 A perifollicular yellowish-orangish halo or yellowish-orangish focal structureless areas resulting from hemosiderin deposits in the dermis may be seen (Figures 1.37B and 1.38B), although in very dark skin they are quite difficult to appreciate.6,20,21 In such patients, however, orangish structureless areas may be observed on the palms/soles in the case of keratoderma.6,20,21 Patchy white scaling is a quite common but unspecific dermoscopic feature of PRP.6,20,21 B

FIGURE 1.37  Classic pityriasis rubra pilaris of the back in an Indian man (A). Yellowish-orangish globular structures are seen on dermoscopy (B).

A

B

FIGURE 1.38  Circumscribed juvenile pityriasis rubra pilaris in an Indian boy (A). Patchy white scales along with perifollicular scaling surrounded by a yellowish-orangish halo (better visible in the inset) are evident on dermoscopic assessment (B).

20

Papulosquamous disorders forms (with restriction to sun-exposed areas in the actinic variant) (Figures 1.40A and 1.41A).8,22 Less common variants include palmo-plantar porokeratosis (Figure 1.42A) and linear porokeratosis (a form resulting from a mosaicism).8,22

1.7 Porokeratosis 1.7.1 Introduction Porokeratosis is a heterogenous group of genodermatoses sharing the presence on histology of the so-called “cornoid lamella”, clinically corresponding to a peripheral keratotic rim with a central groove.8,22 Porokeratosis tends to be more uncommon in dark skin than in fair skin.8,22

1.7.2  Clinical presentation Four main clinical variants are recognized, including disseminated actinic porokeratosis, porokeratosis of Mibelli, linear porokeratosis and disseminated porokeratosis, with the first two forms being the most common.8,22 All of them are characterized by keratotic papules, which gradually enlarge and become atrophic plaques with an elevated keratotic border (Figures 1.39A–1.42A).8,22 Lesions are single or few in porokeratosis of Mibelli (Figure 1.39A) and multiple in disseminated A

1.7.3 Dermoscopy Dermoscopy is very helpful in assisting the diagnosis of porokeratosis, especially in dark-skinned patients as the peripheral keratotic rim is not easy to recognize on clinical examination.6,8 The dermoscopic hallmark is represented by a peripheral keratotic track having two free edges (Figures  1.39B–1.42B) histologically corresponding to the cornoid lamella. Its colour may be white (Figures 1.39B and 1.41B) or brown (Figures  1.40B and 1.42B), with the latter shade being much more common in skin of colour compared with skin of Caucasian patients.6,8 In the centre of the lesions, several poorly specific features may be seen, including white scaling, dotted vessels, keratotic plugs, white or brown structureless areas and brown dots.6,8 B

FIGURE 1.39  Disseminated actinic porokeratosis in an African woman (A). Dermoscopy shows a brown peripheral keratotic track having two free edges; a few white keratotic plugs are also seen in the centre (B).

A

B

FIGURE 1.40  Disseminated actinic porokeratosis in a Caribbean woman (A). Dermoscopy reveals a white peripheral keratotic track having two free edges and a central white structureless area (B).

21

Dermoscopy for skin of colour A

B

FIGURE 1.41  Porokeratosis of Mibelli of the leg in an Indian woman (A). A white-grey keratotic track having two free edges, patchy dotted vessels and white structureless areas is visible on dermoscopic assessment (B).

A

B

FIGURE 1.42  Palmo-plantar porokeratosis (palmar lesions) (A). Dermoscopy shows a brown-grey keratotic track with two free edges; a brown centre and disruption of dermatoglyphics are also evident (B).

1.8  Pityriasis lichenoides 1.8.1 Introduction Pityriasis lichenoides is a group of dermatoses including two main clinic-pathological variants, viz. pityriasis lichenoides et varioliformis acuta (PLEVA) and pityriasis lichenoides chronica (PLC).8,23 Although their exact etiopathogenesis is yet to be understood, it has been speculated that bacterial and viral agents might trigger inflammation via T-cell mediation and immune complex induction.8,23 Both PLEVA and PLC last for an average of 18–20 months.8,23

1.8.2  Clinical presentation Clinical features of PLEVA include asymptomatic or burning/itching erythematous/brownish papules (Figure  1.43A) that often develop a vesiculopustular, haemorrhagic, necrotic, ulcerated or crusted centre as they mature.8,23 They typically involve the trunk and arms with palmo-plantar areas sparing

and often regress spontaneously leaving residual hypopigmentation or varioliform scars.8,23 On the other hand, PLC presents with asymptomatic brownish or skin-coloured papules whose surface becomes diffusely hyperkeratotic/scaling or covered by a single central white scale centrally attached (mica-like scale) that often falls off spontaneously or by scraping (Figures  1.44A and 1.45A).8,23 Lesions are usually distributed over the trunk and extremities and often display a polymorphic appearance with lesions of all stages (because they typically come in crops).8,23 Hypopigmented macules are commonly seen after healing of the inflammatory lesions and may be the sole manifestation of PLC in darker skin phototypes (Figure 1.46A).8,23

1.8.3 Dermoscopy Dermoscopy of mature PLEVA lesions in dark-skinned patients usually demonstrates a central brownish-black crust because of epidermal necrosis surrounded by a peripheral white structureless area (sometimes displaying radial white streaks) with

22 a scaling collarette having an inner free edge (Figure 1.43B), respectively representing acanthosis and hyperkeratosis on histology.6,24 Other less common dermoscopic features include peripheral dotted or linear vessels, haemorrhages and bluishgreyish globules/structureless areas (corresponding to melanin pigment/melanophages in the dermis).6,24 In healing/scarring lesions, white structureless areas due to fibrosis, with or without dotted/linear vessels, are the only visible findings.6,24 The main dermoscopic feature of PLC in skin of colour is represented by the presence of a peripheral white scaling collarette having an inner smooth free edge corresponding

A

Papulosquamous disorders to hyperkeratosis; diffuse or focal brownish structureless areas (due to basal layer pigmentation and dermal hemosiderin deposits) are also often visible (Figure  1.44B).6,24 Other additional dermoscopic findings include brown dots (pigment incontinence in the dermis) (Figure 1.45B), central micaceous scale, haemorrhagic areas and focal dotted and/or linear vessels (Figure  1.44B).6,24 Hypopigmented areas may also be seen at the periphery of healing lesions and are the only dermoscopic feature of postinflammatory residual macules and hypopigmented variants (in this case a peripheral white scaling is also visible) (Figure 1.46B).6,24

B

FIGURE 1.43  Pityriasis lichenoides et varioliformis acuta in an Indian boy (A). Dermoscopy displays a central brownish-black crust surrounded by a peripheral white structureless area and a smooth white scaling collarette having an inner free edge (B).

A

B

FIGURE 1.44  Pityriasis lichenoides chronica in an African woman (A). Dermoscopic examination shows a central mica-like scale surrounded by a peripheral smooth white scale; some haemorrhagic areas are also present (B). (From Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press.)

23

Dermoscopy for skin of colour A

B

FIGURE 1.45  Pityriasis lichenoides chronica in an Indian woman (A). Dermoscopy reveals brown dots (B).

A

B

FIGURE 1.46  Hypopigmented macules in an Indian patient suffering from pityriasis lichenoides chronica (A). Hypopigmented background along with a peripheral collarette scaling is seen on dermoscopy (B).

1.9  Lichen striatus 1.9.1 Introduction Lichen striatus (LS) is a self-limited dermatosis of unknown aetiology presenting as linear lesions distributed along the lines of Blaschko.12 It most commonly occurs in children and spontaneously resolves within 1 year, although it may persist for up to 4 years.12

1.9.2  Clinical presentation The typical clinical presentation consists of skin-coloured, erythematous or hypopigmented (in darker phototypes) papules having a 1–3 mm diameter that coalesce to form a band that progresses down an extremity (more common) or around the trunk (less common) following the lines of Blaschko (Figures 1.47A–1.49A).12 Postinflammatory hypopigmentation is common in skin of colour and may persist for a long time.12

Onychodystrophy is rare and typically restricted to a single nail.12

1.9.3 Dermoscopy On dermoscopic examination, LS in dark-skinned patients typically shows non-follicular, ill-defined, structureless white areas often coalescing to form polycyclic structures (Figures 1.47B–1.49B).6 In terms of clinico-pathological correlation, such areas would be the result of epidermal acanthosis and/or inflammatory reduction of the melanin content.6,12 In very dark-skinned patients, white eccrine sweat gland openings surrounded by brown circles are sometimes seen in the context of the typical white areas (Figure 1.47B).6 This is because of the typical arrangement of the dense inflammatory infiltrate around the eccrine sweat glands and ducts.6,12 White (due to hyperkeratosis) or brown (due to hyperkeratosis and melanin exfoliation) scales may also be seen (Figure 1.48B).6,12

24

Papulosquamous disorders A

B

FIGURE 1.47  Lichen striatus of the left leg in an African boy (A). Dermoscopic assessment shows non-follicular, ill-defined, structureless white areas coalescing (better seen in the inset) to form polycyclic structures (B).

A

B

FIGURE 1.48  Lichen striatus of the left upper arm in an Indian man (A). Confluent ill-defined white structureless areas and patchy white scales are present on dermoscopy (B).

A

B

FIGURE 1.49  Lichen striatus on the right thigh in an Indian man (A). Dermoscopic examination reveals ill-defined white structureless areas along with patchy white and brown scales (B).

25

Dermoscopy for skin of colour

1.10 Lichen simplex chronicus and lichenification 1.10.1 Introduction The term “lichenification” refers to a skin thickening with variable scaling because of repetitive and chronic scratching or rubbing as a consequence of localized chronic pruritus.8 It may occur secondarily to an eczematous dermatitis/other inflammatory itchy conditions or without any underlying skin disease (lichen simplex chronicus – LSC).8

1.10.2  Clinical presentation It presents as a well-defined leathery scaling/keratotic plaque featuring exaggerated skin markings; a brownish hue is quite frequent in dark-skinned patients (Figures  1.50A–1.53A).8 It is often solitary and mainly involves the dorsal aspect of the hands/feet, forearms, nape of the neck, shin of the tibia and anogenital area, although multiple lesions having an asymmetric distribution may also occur.8

1.10.3 Dermoscopy The most frequent dermoscopic features of LSC are diffuse white scaling due to hyperkeratosis and dotted vessels

A

distributed in a patchy or diffuse pattern histologically corresponding to the tips of dilated capillaries in dermal papillae (Figures 1.50B–1.53B).8 Such a vascular pattern is similar to that of psoriasis, yet in LSC, the vessels are usually surrounded by a white halo because of the presence of a thick granular layer, which is typically absent or thinned in psoriasis.8 Notably, in very dark-skinned patients, vessels are more difficult to see. Haemorrhagic areas/dots and crusts, broken hair and superficial erosions are other typical features of LSC, especially on the scalp (Figure  1.53B).8 In skin of colour, dermoscopic examination often also reveals pigmentary structures, including brown structureless areas resulting from basal layer hyperpigmentation and brown/grey dots corresponding to dermal melanophages (Figures 1.50B–1.53B).8 Further possible dermoscopic features of LSC include follicular plugs representing follicular hyperkeratosis and white structureless areas.8 This last finding is more common and marked in dark-skinned patients compared with Caucasian patients and corresponds to dermal fibrosis on histology.8 In secondary forms, the typical feature of the underlying skin disease may be also seen, e.g., yellow scales/crusts in cases secondary to eczematous dermatitis.8

B

FIGURE 1.50  Lichen simplex chronicus of the leg in an Egyptian man (A). Dermoscopy: multifocal white structureless areas, patchy dotted vessels showing white halo, haemorrhagic areas/dots, brown structureless areas and superficial erosions (B).

26

Papulosquamous disorders A

B

FIGURE 1.51  Lichen simplex chronicus of the foot in an Indian man (A). Dermoscopy: white lines, superficial erosions, haemorrhagic areas/dots, patchy white scales and patchy dotted vessels having a white halo (B).

A

B

FIGURE 1.52  Lichen simplex chronicus of the foot in an Indian man (A). Dermoscopy: focal white structureless areas, diffuse white scales, diffuse brown dots and a few haemorrhagic dots (B).

A

B

FIGURE 1.53  Lichen simplex chronicus of the scalp (A). Dermoscopy: white structureless areas, broken hairs, haemorrhagic dots, superficial erosions, white scales, brown structureless areas and sparse dotted vessels (B).

27

Dermoscopy for skin of colour

(especially in darker phototypes) papules that often tend to coalesce (Figure  1.54A).25 The elbows, dorsal aspect of the hands and knees are the most commonly involved areas.25

1.11  Frictional lichenoid dermatitis 1.11.1 Introduction Frictional lichenoid dermatitis (FLE) is a probably underreported condition related to repeated friction/trauma that has been speculated to be associated with sunlight exposure and atopic dermatitis.25

1.11.2  Clinical presentation

1.11.3 Dermoscopy Dermoscopy of FLE reveals a whitish background due to acanthosis and hypergranulosis and uniform dotted vessels histologically corresponding to the tip of dilated/elongated vessels in dermal papillae (Figure 1.54B).15 Haemorrhagic dots/spots and crusts may also be seen.15

From a clinical point of view, FLE typically manifests as multiple, pinhead-sized, skin-coloured or hypopigmented

A

B

FIGURE 1.54  Frictional lichenoid dermatitis of the back of the hand in an Indian boy (A). Ill-defined white structureless areas and uniform dotted vessels (B).

REFERENCES

1. Geng A, McBean J, Zeikus PS, McDonald CJ. Psoriasis. In: Dermatology for Skin of Colour (Kelly AP, Taylor SC, eds), 1st edn. New York: McGraw-Hill Medical, 2009:139–46. 2. Thorpe R, Pandya AG. Psoriasis. In: Dermatology Atlas for Skin of Colour (Jackson-Richards D, Pandya AG, eds), 1st edn. Berlin: Springer-Verlag, 2014:131–8. 3. Errichetti E, Stinco G. Dermoscopy in general dermatology: A  practical overview. Dermatol Ther (Heidelb) 2016;6:471–507. 4. Errichetti E, Stinco G. The practical usefulness of dermoscopy in general dermatology. G Ital Dermatol Venereol 2015;150:533–46. 5. Errichetti E. Dermoscopy of inflammatory dermatoses (inflammoscopy): An up-to-date overview. Dermatol Pract Concept 2019;9:169–80. 6. Errichetti E, Ankad BS, Sonthalia S, et  al. Dermoscopy in general dermatology (non-neoplastic dermatoses) in skin of colour: A  comparative retrospective study by the International Dermoscopy Society. Eur J Dermatol 2020. doi: 10.1684/ejd.2020.3928 7. Nwako-Mohamadi MK, Masenga JE, Mavura D, Jahanpour OF, Mbwilo E, Blum A. Dermoscopic features of psoriasis,

lichen planus, and pityriasis rosea in patients with skin type IV and darker attending the regional dermatology training Centre in Northern Tanzania. Dermatol Pract Concept 2019;9:44–51. 8. Lallas A, Errichetti E. Papulosquamous disorders. In: Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press, 2018:2–46. 9. Desai N, Alexis AF. Atopic dermatitis and other eczemas. In: Dermatology for Skin of Colour (Kelly AP, Taylor SC, eds), 1st edn. New York: McGraw-Hill Medical, 2009:163–6. 10. Jackson-Richards D. Atopic dermatitis. In: Dermatology Atlas for Skin of Colour (Jackson-Richards D, Pandya AG, eds), 1st edn. Berlin: Springer-Verlag, 2014:101–8. 11. Bridges KH. Lichen planus. In: Dermatology for Skin of Colour (Kelly AP, Taylor SC, eds), 1st edn. New York: McGraw-Hill Medical, 2009:152–7. 12. Condie D, Pandya AG. Lichen planus, nitidus, and striatus. In: Dermatology Atlas for Skin of Colour (Jackson-Richards D, Pandya AG, eds), 1st edn. Berlin: Springer-Verlag, 2014:115–22. 13. Bridges KH. Lichen nitidus. In: Dermatology for Skin of Colour (Kelly AP, Taylor SC, eds), 1st edn. New York: McGraw-Hill Medical. 2009:158.

28 14. Modi S, Harting M, Metry D. Lichen nitidus actinicus: A  distinct facial presentation in 3 pre-pubertal AfricanAmerican girls. Dermatol Online J 2008;14:10. 15. Errichetti E, Stinco G. Comment on “dermatoscopic features of lichen nitidus”. Pediatr Dermatol 2018;35:879–80. 16. Jakhar D, Grover C, Kaur I, Sharma S. Dermatoscopic features of lichen nitidus. Pediatr Dermatol 2018;35:866–7. 17. Shabazz DR. Pityriasis rosea. In: Dermatology for Skin of Colour (Kelly AP, Taylor SC, eds), 1st edn. New York: McGraw-Hill Medical, 2009:147–51. 18. Jackson-Richards D. Pityriasis rosea. In: Dermatology Atlas for Skin of Colour (Jackson-Richards D, Pandya AG, eds), 1st edn. Berlin: Springer-Verlag, 2014:123–6. 19. Jacyk WK. Pityriasis rubra pilaris in black South Africans. Clin Exp Dermatol 1999;24:160–3. 20. Jha AK, Lallas A, Sonthalia S, Jhakar D, Udayan UK, Chaudhary RKP. Differentiation of pityriasis rubra

Papulosquamous disorders pilaris from plaque psoriasis by dermoscopy. Dermatol Pract Concept 2018;8:299–302. 21. Nair PA, Sheth N. Dermoscopy of juvenile circumscribed pityriasis rubra pilaris. Indian Dermatol Online J 2018;9:474–6. 22. LeCourt AP. Porokeratosis. Emedicine.medscape.com. 2020 (Accessed 19 December 2020) 23. Wang A, Pandya AG. Pityriasis lichenoides chronica. In: Dermatology Atlas for Skin of Colour (Jackson-Richards D, Pandya AG, eds), 1st edn. Berlin: Springer-Verlag, 2014:127–30. 24. Ankad BS, Beergouder SL. Pityriasis lichenoides et varioliformis acuta in skin of colour: New observations by dermoscopy. Dermatol Pract Concept 2017;7:27–34. 25. Sardana K, Goel K, Garg VK, et al. Is frictional lichenoid dermatitis a minor variant of atopic dermatitis or a photodermatosis. Indian J Dermatol 2015;60:66–73.

2 Other papulonodular disorders

Other papulonodular disorders

Dermoscopy for skin of colour

Enzo Errichetti, Balachandra Ankad, Bengu Nisa Akay, Richard Usatine and Aimilios Lallas

2.1  Papular acantholytic dermatoses 2.1.1 Introduction The main papular acantholytic dermatoses include Grover’s disease, Darier’s disease and papular acantholytic dermatosis of the genitocrural area (PADGA).1,2 Such conditions typically share the presence of acantholytic dyskeratotic changes on histology.1,2 Although Grover’s disease and PADGA are considered sporadic conditions, Darier’s disease is an autosomal dominant inherited genodermatosis due to mutations in the gene ATP2A2 (encoding an intracellular calcium pump).1,2

2.1.2  Clinical presentation All the previously-mentioned conditions present with itchy or asymptomatic papules that mainly differ in terms of colour and localization.1,2 In detail, in both Darier’s disease and Grover’s disease, papules are brown and may be hyperkeratotic (especially in the former), yet affected areas include seborrheic areas, skin creases and the trunk in the former (Figures 2.1A and 2.2A) and the central back/mid chest in the latter (Figure  2.3A).1,2 Moreover, postinflammatory white macules of the skin (Figure 2.1A) and macerated/eroded plaques of the folds (Figure 2.2A) are also present in Darier’s disease. On the other hand, PADGA is typified by white papules involving the genital areas, perianal area and inguinal folds (Figure 2.4A).1,2 Additionally, Darier’s disease occurs earlier (6–20 years) than Grover’s disease and PADGA (both of them usually occurring

A

in adulthood) and is typically associated with nail abnormalities, acral skin lesions and mucous membrane changes.1,2

2.1.3 Dermoscopy Dermoscopy displays a similar pattern in Darier’s disease, Grover’s disease (Darier-like histological subtype)3,4 and PADGA (authors’ personal observations), namely a central polygonal or star-shaped brown area surrounded by a white halo (Figures  2.1B, 2.2B and 2.4B). From a dermoscopichistological correlation point of view, the central brown area corresponds to a compact keratotic mass mixed with serum (resulting from exudation due to acantholysis) and melanin (due to melanin exfoliation, which is more common in skin of colour), whereas the peripheral white area is related to epidermal acanthosis.3,4 Additionally, in dark-skinned patients, all such conditions often feature a perilesional grey-brown pigmentation resulting from postinflammatory pigmentation (authors’ personal observations). Of note, Darier’s disease may also show star-shaped/ polygonal white areas in healed skin areas (postinflammatory hypopigmentation) (Figure  2.1B) as well as star-like/linear and parallel erosions over a white background (with or without white shiny lines) (Figure 2.2B) similar to the pattern seen in Hailey-Hailey disease. Less specific findings visible in both Darier’s disease and Grover’s disease include white scales and yellow/brown crusts, which may be the only dermoscopic structures seen in the latter condition in its spongiotic histological variant (Figure 2.3B).4

B

FIGURE 2.1  Darier’s disease in an African American woman (A). Dermoscopic assessment displays multiple polygonal and star-shaped brownish/ reddish areas surrounded by white halos and peripheral grey-brown pigmentation; white polygonal/star-shaped areas resulting from postinflammatory hypopigmentation are also seen (B). DOI: 10.1201/9780367816483-2

30 A

Other papulonodular disorders B

FIGURE 2.2  Macerated and eroded plaque in the left submammary fold (previous patient) (A). Dermoscopy shows star-like/linear and parallel erosions over a white background, similar to the pattern seen in Hailey-Hailey disease; white shiny lines are also visible (B).

A

B

FIGURE 2.3  Grover’s disease (spongiotic variant) of the back in a Middle Eastern man (A). Dermoscopy reveals white/brown scales/crusts with a peripheral brown halo (B).

A

B

FIGURE 2.4  Papular acantholytic dermatosis of the genitocrural area in a South Asian man (A). Dermoscopic examination shows multiple starshaped areas (white arrows) surrounded by white halos and peripheral brown pigmentation (B).

31

Dermoscopy for skin of colour

and the lesions may become weepy, crusted and secondarily infected.1 In dark skin, healing often leaves significant postinflammatory hypo- or hyperpigmented macules and/or patches.1

2.2  Papular urticaria 2.2.1 Introduction Papular urticaria (PU) is a frequent condition due to a hypersensitivity reaction to the bites of several insects, such as mosquitoes, sandflies, fleas and bedbugs; it is more common among children.1

2.2.2  Clinical presentation PU manifests as chronic or recurrent crops of asymmetrically distributed itchy skin-coloured papules and papulovesicles that are typically localized on exposed areas of the body (Figures 2.5A and 2.6A), although covered areas may also be involved.1 Scratching may produce erosions and ulcerations, A

2.2.3 Dermoscopy Dermoscopy may be helpful to show the central haemorrhagic punctum corresponding to the site of the insect bite (Figure  2.5B) or display one or multiple haemorrhagic spots representing extravasated erythrocytes in the dermis (commonly seen on histologic examination in PU).1 Additional dermoscopic features include erosions, roundish/angulated brown/yellow crusts and white structureless areas (healing lesions) (Figure  2.6B).1 This last finding is more frequent in skin of colour because of the common occurrence of postinflammatory dyschromia in darker phototypes.1

B

FIGURE 2.5  Papular urticaria in a North African boy (A). A central haemorrhagic punctum is visible on dermoscopy (B).

A

B

FIGURE 2.6  Papular urticaria in an African woman (A). Dermoscopic assessment displays roundish/angulated brown crusts surrounded by white halos (B).

32

Other papulonodular disorders

2.3.3 Dermoscopy

2.3  Prurigo nodularis 2.3.1 Introduction Prurigo nodularis (PN) is a chronic condition whose lesions are induced by skin picking and scratching.1,5 Although it may occur at any age, middle-aged and elderly people seem to be affected more frequently; common associations include atopic dermatitis and systemic causes of pruritus.1,5

2.3.2  Clinical presentation PN in dark skin manifests as 0.5–3 cm in diameter, discrete, skin-coloured or brownish nodules whose surface may be hyperkeratotic or excoriated (Figures  2.7A–2.9A).1,5 It generally involves extensor surfaces of the arms, legs and trunk with a symmetric pattern; the palms, soles, face and creases are usually not affected.1,5 Additionally, sparing of the centre of the back (“butterfly sign”) and a linear arrangement are considered typical of PN.1,5 Postinflammatory hyper- or hypopigmentations are common in darker phototypes (Figure 2.10A).1,5 A

The dermoscopic hallmark of PN consists of peripheral, radial, white striae over a brownish background (the so-called “white starburst” pattern) (Figures 2.7B and 2.8B).6,7 Ulceration/erosion, crusting, white hyperkeratosis/scales, broken hairs, follicular plugs, white structureless areas/globules, haemorrhagic dots/globules and/or dotted/globular vessels (often surrounded by a white halo) may also be seen in the centre of the lesions (Figures  2.7B–2.9B).6,7 A  white peripheral scaling collarette with an inner free edge is sometimes evident at the periphery (Figures 2.7B and 2.8B). White structures on dermoscopy histologically correspond to dermal thickened collagen fibres, which typically feature a vertical arrangement in the papillary dermis, thereby appearing like whitish striae when the lesions are observed from above (through the dermoscope), especially at the periphery, where the contrast with hyperpigmented skin is easier to appreciate.6,7 Of note, dermoscopy may also come in handy in retrospective diagnosis as healing/non-active lesions often retain the aforementioned “white starburst” pattern (Figure 2.10B).6,7

B

FIGURE 2.7  Prurigo nodularis in an African atopic boy (A). Dermoscopy shows a bright white area having peripheral radial linear projections (“white starburst” pattern) surrounded by a white scaling collarette having an inner free edge and a brown halo (B).

A

B

FIGURE 2.8  Prurigo nodularis in an African boy (A). Dermoscopic examination reveals peripheral radial white striae and white collarette scaling along with uniform dotted vessels surrounded by a white halo, sparse brown dots and a few white follicular plugs in the centre (B).

33

Dermoscopy for skin of colour A

B

FIGURE 2.9  Prurigo nodularis in an African American girl (A). Dermoscopy: patchy dotted vessels having a white halo in the centre of the lesion and peripheral brown pigmentation (B).

A

B

FIGURE 2.10  Healing phases of prurigo nodularis in an African woman (A). The white starburst is visible on dermoscopic examination, thereby facilitating the retrospective diagnosis (B).

2.4  Acquired perforating dermatoses 2.4.1 Introduction The term “acquired perforating dermatoses” (APD) refers to a group of disorders characterized by invagination of the epidermis (which may be follicular or perifollicular) and extrusion of dermal material, whose composition varies according to the histological subtype (i.e., collagen bundles in acquired reactive perforating collagenosis [ARPC], elastic fibres in acquired elastosis perforans serpiginosa [AEPS], amorphous dermal material and/or keratin in Kyrle’s disease [KD] and degenerating collagen and extracellular matrix in perforating folliculitis [PF] – overlaps are, however, not rare).1 APD are often associated with chronic renal disease or diabetes mellitus.1

2.4.2  Clinical presentation APD manifest as itchy, round, umbilicated, skin-coloured or hyperpigmented papules and nodules having a central crust

or keratotic plug, most commonly involving the extensor surfaces of the extremities and the trunk (Figures 2.11A and 2.12A).1

2.4.3 Dermoscopy Dermoscopic examination of ARPC, PF and KD in darkskinned patients shows a similar appearance, consisting of the presence of three concentric areas (“trizonal concentric” pattern), with a central yellow/brown-grey structureless area (I) surrounded by a white keratotic collarette (II) and a white halo (III) (Figures 2.11B and 2.12B).7,8 Different from fair-skinned patients,1,9 in darker phototypes, vessels are not usually seen, whereas a peripheral brown halo is often appreciated (giving rise to four concentric areas) (Figure  2.12B).7,8 Dermoscopy of AEPS has been reported only in Caucasian patients and displays central whitish structureless area with a crown of arborizing vessels or central pink-yellow discolouration with peripheral brownish crusted papules surrounded by a white halo and arranged in an “archipelago” pattern.10

34

Other papulonodular disorders A

B

FIGURE 2.11  Perforating folliculitis in an African man (A). Dermoscopy displays a “trizonal concentric” pattern, with a central yellowish structureless area surrounded by a white keratotic collarette and a white halo; a peripheral brown halo is also evident (giving rise to four concentric areas) (B).

A

B

FIGURE 2.12  Acquired reactive perforating collagenosis in an Indian man (A). Four concentric areas are visible on dermoscopy, namely central yellow keratotic area, white keratotic collarette, white halo and peripheral brown pigmentation (B).

REFERENCES 1. Errichetti E, Lallas A, Ioannides D. Other papulonodular disorders. In: Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press, 2018:47–55. 2. Al-Muriesh M, Abdul-Fattah B, Wang X, Zhao M, Chen S, Huang C. Papular acantholytic dyskeratosis of the anogenital and genitocrural area: Case series and review of the literature. J Cutan Pathol 2016;43:749–58. 3. Errichetti E, Stinco G, Lacarrubba F, Micali G. Dermoscopy of Darier’s disease. J Eur Acad Dermatol Venereol 2016;30:1392–4. 4. Errichetti E, De Francesco V, Pegolo E, Stinco G. Dermoscopy of Grover’s disease: Variability according to histological subtype. J Dermatol 2016;43:937–9. 5. LeCourt AP. Purigo nodularis. Emedicine.medscape.com. 2020 (Accessed 19 December 2020)



6. Errichetti E, Piccirillo A, Stinco G. Dermoscopy of prurigo nodularis. J Dermatol 2015;42:632–4. 7. Errichetti E, Ankad BS, Sonthalia S, et  al. Dermoscopy in general dermatology (non-neoplastic dermatoses) in skin of colour: A  comparative retrospective study by the International Dermoscopy Society. Eur J Dermatol 2020. doi: 10.1684/ejd.2020.3928 8. Ramirez-Fort MK, Khan F, Rosendahl CO, Mercer SE, Shim-Chang H, Levitt JO. Acquired perforating dermatosis: A  clinical and dermatoscopic correlation. Dermatol Online J 2013;19:18958. 9. Errichetti E, Stinco G. Dermoscopy in general dermatology: A  practical overview. Dermatol Ther (Heidelb) 2016;6:471–507. 10. Navarrete-Dechent C, Puerto Cd, Bajaj S, Marghoob AA, González S, Jaque A. Dermoscopy of elastosis perforans serpiginosa: A useful tool to distinguish it from granuloma annulare. J Am Acad Dermatol 2015;73:e7–e9.

3 Non-infectious granulomatous disorders and connective tissue diseases Granulomatous and connective tissue

Dermoscopy for skin of colour

Enzo Errichetti, Ahmed Sadek, Balachandra Ankad, Dalia Hossam, Abhijeet Kumar Jha, Shekhar Neema, Vinay Keshavamurthy, Horacio Cabo, Nkechi Enechukwu, Adebola Ogunbiyi, Aimilios Lallas and Payal Chauhan

3.1 Sarcoidosis

3.1.3 Dermoscopy

3.1.1 Introduction

The dermoscopic hallmark of the various forms of sarcoidosis classically consists of the presence of orange structureless areas histologically corresponding to the dense and compact granulomatous infiltrate in the dermis (“mass effect”) (Figure  3.1B).1,4–6 Notably, in darker phototypes, such areas are frequently more subtle and sometimes display a yellowish hue (Figure 3.2B).1,4–7 Applying a slight pressure on the skin may enhance their visualization because of the reduction of erythema, yet their global prevalence is, anyway, lower than in fair-skinned patients because of the more intense pigmentation that masks them.1,4–7 Orange/yellowish structureless areas may be focally distributed or diffuse as a background, with the latter being more typical of sarcoidosis compared with other granulomatous dermatoses.1,4–7 Branching vessels are the second most common dermoscopic feature in sarcoidosis (Figure 3.1B), although they are seen less commonly compared with Caucasian patients.1,4–7 Interestingly, such vascular structures are typically well focused as granulomas push the dermal vessels upward (closer to the skin surface), thereby appearing sharper.1,4–7 Additional dermoscopic findings include white scales, focal white structureless areas, white globules or lines and focal brown structureless areas.7

Sarcoidosis is a systemic granulomatous condition of unknown aetiology that is histologically typified by noncaseating, “naked” granulomas (epithelioid granulomas with few surrounding lymphocytes).1–3 The lungs, skin, eyes and lymph nodes are the most commonly involved districts, yet almost any organ may be affected.1–3

3.1.2  Clinical presentation Cutaneous manifestations of sarcoidosis are divided into nonspecific/reactive (e.g., erythema nodosum) and specific (histologically characterized by “naked” granulomas) lesions.1–3 Specific sarcoidal lesions in dark skin include asymptomatic red/brown papules, nodules, patches and/or plaques most commonly involving the face (Figure 3.1A), neck, upper back and extremities (Figure 3.2A).1–3 The surface of the lesions may be smooth, atrophic, scaly, hyperkeratotic, or ulcerated.1–3 More uncommon clinical variants do exist, such as subcutaneous sarcoidosis, ichthyosis-like sarcoidosis, lichenoid sarcoidosis, scar sarcoidosis, lupus pernio and hypopigmented sarcoidosis, with the last two forms being more common in skin of colour.1–3

A

B

FIGURE 3.1  Nodular sarcoidosis of the face in an Indian man (A). Dermoscopy shows diffuse structureless areas along with focused linear-branched vessels and patchy white scales (B).

DOI: 10.1201/9780367816483-3

36 A

Granulomatous and connective tissue B

FIGURE 3.2  Papular sarcoidosis of the right arm in an Indian man (A). Dermoscopic examination reveals yellowish structureless areas and patchy white scales (B).

3.2  Necrobiosis lipoidica 3.2.1 Introduction Necrobiosis lipoidica (NL) is an uncommon chronic idiopathic granulomatous disorder characterized by necrobiotic degenerative changes of dermal collagen that mainly affects young and middle-aged adults with a female sex predominance.1,2,8 A possible association with diabetes and thyroid dysfunction may be seen in a minority of cases.1,2,8 Notably, such a condition is quite rare in dark-skinned patients.1,2,8

3.2.2  Clinical presentation In pigmented skin, NL begins as brown firm papules gradually enlarging to form plaques with raised reddish-brown borders and a waxy yellowish-brown atrophic centre; central prominent telangiectasias and/or ulcerations may also be seen (Figures  3.3A–3.5A).1,2,8 NL typically affects the pretibial area with a unilateral or bilateral distribution, although the scalp, upper extremities and face may also be involved.1,2,8 Altered sensations and partial alopecia are commonly observed in affected areas, whereas pain and pruritus are less frequent.1,2,8

3.2.3 Dermoscopy The most characteristic dermoscopic features of necrobiosis lipoidica are seen at the centre of the lesions and include structureless yellowish-orangish areas, histologically corresponding to the granulomatous infiltrate and lipid deposits (often responsible for a yellower hue compared with other granulomatous diseases), and well-focused vessels having a morphology that varies according to the disease stage (Figures  3.3B and 3.4B).1,4–7 In detail, dotted, globular, comma-shaped and glomerular vessels are more common in the early stages, whereas network-shaped, linear and hairpin-like vessels are more frequent in the more developed (mature) lesions and branching-serpentine vessels (whose diameter typically decreases from the centre to the periphery of the lesion) in advanced lesions.1,4–7 Of note, vessels in NL are typically well-focused as the epidermal atrophy makes the vessels closer to the skin surface, so that they appear sharper and larger.1,4–7 A dermoscopic feature of NL that is mainly seen in skin of colour is represented by brown structureless areas and a brown network (Figures 3.4B and 3.5B), both in the centre and periphery of the lesion.1,4–7 Additional dermoscopic findings include ulcerations, crusts, white scales and white structureless areas due to dermal fibrosis (especially in long-standing lesions) (Figure 3.5B).1,4–7

37

Dermoscopy for skin of colour A

B

FIGURE 3.3  Necrobiosis lipoidica of the right thigh in a North African woman (A). Typical focused branching serpiginous vessels, structureless yellowish and brown areas and white scales are visible on dermoscopy (B).

A

B

FIGURE 3.4  Necrobiosis lipoidica of the leg in an Indian woman (A). Dermoscopy: focused branching serpiginous vessels whose diameter reduces towards the periphery (better seen in the inset) and brown areas; faint structureless yellowish areas are also present (B).

A

B

FIGURE 3.5  Ulcerative long-standing necrobiosis lipoidica in an Indian man (A). White structureless areas and a brown network is evident on dermoscopic assessment (B).

38

3.3  Granuloma annulare 3.3.1 Introduction Granuloma annulare is a relatively frequent, benign, inflammatory condition of uncertain aetiology that may show several histological patterns, including “interstitial”, “palisading granuloma”, sarcoidosis-like and mixed, with the first two forms being by far the most common.1,9

3.3.2  Clinical presentation Granuloma annulare manifests as localized or generalized, asymptomatic, skin-coloured to violaceous, non-scaly papules/nodules, which may be sparse (Figure 3.6A) or coalesce into annular or roundish plaques (Figures 3.7A and 3.8A); less common distinct clinicopathological variants include subcutaneous, perforating and patch-type forms.1,9 A

Granulomatous and connective tissue

3.3.3 Dermoscopy The most frequent dermoscopic findings of granuloma annulare include focal/diffuse orangish-yellowish structureless areas, focal/diffuse white structureless areas, erythema and sparse dotted or linear/linear curved vessels (Figures 3.6B–3.8B).6,10 Importantly, orangish-yellowish areas are typically seen only in the “palisading granuloma” histological variant as they are related to the presence of a compact granulomatous infiltrate (Figures 3.7B and 3.8B).6,10 On the other hand, white areas, histologically corresponding to dermal fibrosis, and vessels may be seen in granuloma annulare regardless the histological subtype.6,10 Of note, differently from sarcoidosis, vascular structures in granuloma annulare are usually blurred/subtle (Figure 3.7B), thereby being difficult to appreciate in darker phototypes (Figures 3.6B–3.8B).7 Brown structureless areas and/or network are also not uncommonly seen in dark-skinned patients (Figures 3.6B–3.8B), but they are poorly specific.7 B

FIGURE 3.6  Granuloma annulare (interstitial histological variant) of the dorsal aspect of the feet in an African woman (A). Dermoscopy only reveals a brownish background along with focal white structureless areas (arrows) (B).

A

B

FIGURE 3.7  Granuloma annulare (palisading histological variant) of the right arm in an Indian man (A). Yellowish structureless areas, focal brown structureless areas and blurred linear-irregular vessels are evident on dermoscopic examination (B).

39

Dermoscopy for skin of colour A

B

FIGURE 3.8  Granuloma annulare (palisading histological variant) of the dorsal aspect of the right hand in an African boy (A). A subtle yellowish background along with brown structureless areas and fine white scales are visible on dermoscopy (B).

A

B

FIGURE 3.9  Lupus miliaris disseminatus faciei in an Indian female. Clinical appearance (A). Dermoscopy reveals focal, yellowish-orange, structureless areas around follicles with diffuse erythema and vessels; prominent keratotic plugs and scales are also seen (B).

3.4  Lupus miliaris disseminatus faciei

3.5  Lupus erythematosus

3.4.1 Introduction

3.5.1 Introduction

Lupus miliaris disseminatus faciei (LMDF), also known as acne agminata, is a relatively rare granulomatous dermatosis that is thought to be an inflammatory reaction to destroyed hair follicles.11

Lupus erythematosus (LE) is a group of inflammatory autoimmune diseases pathogenetically related to genetic, hormonal and environmental factors that may affect multiple organs, including the skin.2,14,15 In general, LE is reported to affect African Americans and Hispanics more frequently than Caucasian, Asian and Latin Americans.2,15 Three main subtypes of cutaneous LE are described, i.e., chronic cutaneous LE (CCLE), subacute cutaneous LE (SCLE) and acute cutaneous LE (ACLE), with the first one being the most common form in dark-skinned patients.2,14,15

3.4.2  Clinical presentation LMDF in skin of colour typically presents with yellowish-red to brown papules over the central part of the face, including on and around the eyelids, cheeks and nose (Figure 3.9A).11 The lesions tend to heal with scars over a period of 12–24 months.11

3.4.3  Dermoscopy Dermoscopic examination of LMDF displays focal, structureless, yellowish-orange areas typically surrounding follicular keratotic plugs along with diffuse erythema (Figure  3.9B); scales and vessels may also be seen.12,13

3.5.2  Clinical presentation Sun-induced faint erythematous patches or plaques affecting malar areas with nasolabial folds sparing is the classical presentation of ACLE in skin of colour (Figure  3.10A).2,15

40 Residual dyspigmentation may be seen in darker-skinned subjects.2,15 Broken and thinned hairs at the front hairline (“lupus hair”), nail apparatus changes (periungual erythema and red lunula) and multiple, erythematous confluent macules and papules in photo-exposed areas are other possible ACLE-specific manifestations (Figure 3.11A).2,15 SCLE is quite rare in skin of colour and typically presents as erythematous scaly papules evolving into either an annular or a papulosquamous form, most commonly involving the upper chest and extensor aspects of the upper extremities.2,15 Finally, CCLE has four main clinical subtypes, including discoid LE (DLE), LE tumidus, lupus panniculitis and chilblain lupus, with the first variant being by far the most frequent in dark skin phototypes.2,15 DLE mainly affects the scalp, face, lips and ears with erythematous/brownish papules evolving into plaques with adherent scales that heal with atrophy, hypo-/hyperpigmentation and scarring, which are responsible for significant disfigurement in dark-skinned patients (Figures 3.12A–3.15A).2,15 Scarring alopecia is seen in hair-bearing areas (Figure  3.14A). Other less common variants of DLE include generalized DLE, in which lesions affect above and below the neck level, and hypertrophic DLE.2,15

3.5.3 Dermoscopy Dermoscopy in skin of colour may be useful in assessing both ACLE and DLE. The dermoscopic appearance of malar erythema is quite unspecific, being characterized only by a faint erythema and fine white scaling, with or without follicular plugs, dotted/linear vessels and peppering (authors’ personal observations) (Figure  3.10B). However, it may still come in handy in helping differentiate such a condition from its main differential diagnoses as they typically display different features (i.e., rosacea, dermatomyositis and seborrheic dermatitis – see specific chapters). The nail apparatus may also

A

Granulomatous and connective tissue feature some changes on dermoscopy, such as whitish areas of the proximal nailfold or longitudinal melanonychia caused by melanocytic activation due to nail matrix inflammation. Unlike dermatomyositis and systemic sclerosis, dermoscopy of the proximal nailfold of ACLE patients does not display relevant findings (Figure 3.11B), apart from tortuous vessels with an abnormal morphology. Dermoscopic assessment of DLE reveals several findings that vary according to the disease stage.5,7,14 In active lesions, white/brown follicular plugs, histologically corresponding to follicular hyperkeratosis (mixed to melanin in the case of brown plugs), on a reddish/brownish background are the most common features, along with diffuse or central white scaling (which is particularly marked in hypertrophic DLE) (Figures 3.12B and 3.13B). 5,7,14 Vascular structures, such as peripheral dotted, linear-curved, linear and linear-branching vessels (Figures 3.12B and 3.13B), are seen less commonly compared with Caucasian patients. 5,7,14 Over time, the pigmentary structures are also often visible in dark-skinned patients, especially at the periphery of the lesions, including brown perifollicular circles/semicircles and structureless areas (sometimes forming a brown pseudonetwork on the face) (Figures  3.12B–3.14B), histologically corresponding to basal layer hyperpigmentation, as well as brown and/or grey dots/globules representing pigment incontinence in the dermis. 5,7,14 In long-standing lesions, dermal fibrosis gives rise to white bright areas on dermoscopy that may be structureless, linear or globular (this last morphology is more common in skin of colour compared with Caucasian patients and is related to follicular fibrosis) (Figures  3.13B and 3.14B). 5,7,14 Lips DLE (Figures 3.15B) typically shows the same features as cutaneous DLE apart from follicular plugs, which are obviously absent because of the lack of follicles in this area; on the other hand, erosions are more commonly seen in this district (authors’ personal observations).

B

FIGURE 3.10  Systemic lupus erythematosus involving the face in a North African woman (A). Dermoscopy: faint erythema, fine white scaling and a few dotted and linear vessels (better seen in the inset) (B). (Courtesy of Awatef Kelati, MD – Casablanca, Morocco.)

41

Dermoscopy for skin of colour A

B

FIGURE 3.11  Hands of the previous patient (A). Dermoscopy: whitish areas of the proximal nailfold; unlike dermatomyositis and systemic sclerosis, no dilated vessels (megacapillaries) are seen (B). (Courtesy of Awatef Kelati, MD – Casablanca, Morocco.)

A

B

FIGURE 3.12  Discoid lupus erythematosus in a North African man (A). Dermoscopic examination reveals grey-brown follicular plugs (better seen in the inset) along with brown-grey scaling, erythema and subtle linear vessels at the periphery (B).

A

B

FIGURE 3.13  Chronic dyschromic lesions in a case of extra-facial discoid lupus erythematosus in an Indian woman (A). Dermoscopy: white-grey follicular dots over a bright white background as well as peripheral brown areas and subtle, unfocused linear/dotted vessels (B).

42

Granulomatous and connective tissue

A

B

FIGURE 3.14  Scarring lesions in a case of facial discoid lupus erythematosus in an African woman (A). Dermoscopy: white bright structureless areas along with brown structureless areas and perifollicular brown-grey dots; bright follicular white dots/globules are also seen and represent follicular fibrosis (B).

A

B

FIGURE 3.15  Discoid lupus erythematosus of the lips in an Indian woman (A). Dermoscopic examination displays erosive areas surrounded by a white rim and peripheral grey-brown dots and structureless areas (B).

3.6 Dermatomyositis 3.6.1 Introduction Dermatomyositis is an idiopathic inflammatory myopathy typically involving large proximal muscle groups (e.g., the upper arms and thighs) and commonly causing peculiar skin manifestations that may occur in both children and adults.14,16 The joints, oesophagus, lungs and heart are other organs that may be affected.14,16 Skin changes may be concomitant, precede, or

follow muscle involvement or be the only manifestations of the disease (amyopathic dermatomyositis).14,16

3.6.2  Clinical presentation Several skin changes have been reported in dermatomyositis, with “pathognomonic” (Gottron’s papules, heliotrope rash and Gottron’s sign) and “characteristic” (shawl sign/V-sign, nailfold changes, photosensitive poikiloderma and scalp scaly dermatosis) (Figures  3.16A, 3.17A, 3.19A–3.21A) findings being

43

Dermoscopy for skin of colour the most important ones from a diagnostic point of view.14,16 Other less common skin lesions include periorbital oedema/ facial swelling, pruritus, cutaneous vasculitis, panniculitis, calcinosis, zebra-like erythema (Figure  13.18A), erythroderma, vesiculo-bullous manifestations, follicular hyperkeratosis, “mechanic’s hands”, “holster” sign and “callosity feet”.14,16 Of note, in very dark phototypes, the typical purple hue of dermatomyositis erythema is lacking and hyperpigmentation is often the only finding that may be appreciated.14,16

3.6.3  Dermoscopy Several “pathognomonic” and “specific” cutaneous manifestations of dermatomyositis may benefit from dermoscopic examination, mainly including Gottron’s papules, heliotrope rash, Gottron’s sign, shawl sign/V-sign, scalp scaly dermatosis, nailfold changes and cutaneous calcinosis.14 In detail, Gottron’s papules show variable features based on their stage, with early/active lesions often displaying a pinkish background with or without dotted/linear-irregular vessels (due to dermal vasodilation) and central scaling/crusting (hyperkeratosis/ necrosis) and advanced lesions featuring whitish areas (mucin depositions/fibrosis).14 In very dark phototypes, vessels may be difficult to appreciate and brown hyperpigmentation is often seen, especially in advanced phases (postinflammatory basal cell layer hyperpigmentation) (Figure 3.16B) (authors’ personal observations). Heliotrope rash, Gottron’s sign and shawl sign/V-sign (but also other erythematous lesions of dermatomyositis) usually

A

show more or less focused reticular/linear-irregular vessels, representing the ectatic subpapillary vascular plexus through the atrophic epidermis and scaling (due to hyperkeratosis).14 However, in dark skin, vessels may be difficult to appreciate and a purplish background with perifollicular white areas (due to perifollicular mucin deposits) is the only feature seen (Figures  3.17B and 3.18B) (authors’ personal observations). Additionally, in very dark phototypes, erythema is replaced by a brown background (related to basal cell layer hyperpigmentation) with or without brown dots (resulting from dermal pigment incontinence) (Figure  3.19B) (authors’ personal observations). Scalp scaly dermatosis mainly displays enlarged tortuous capillaries, erythematous violaceous areas and scaling (perifollicular casts and interfollicular scales); less common findings include bushy capillaries, interfollicular/perifollicular pigmentation and hair loss.14 Proximal nailfold dermoscopy may reveal relevant findings, viz. dilated vessels (including giant capillaries), haemorrhagic spots, thickened/hyperkeratotic cuticle over an erythematous background, and whitish areas (likely due to dermal oedema/mucin deposits/fibrosis) (Figure  3.20B).14 In very dark-skinned patients, vessels may be difficult to see and white areas, often associated with brown hyperpigmentation, are the only visible finding (Figure 3.21B) (authors’ personal observations). Finally, dermoscopy may be of aid in recognizing cutaneous calcinosis, which usually shows bright white areas over a pinkish background, with or without vessels.14

B

FIGURE 3.16  Dermatomyositis in an Indian man (Gottron’s papules) of the dorsal aspect of the right hand (A). Dermoscopy shows multifocal white structureless areas along with brown hyperpigmentation (B).

44 A

Granulomatous and connective tissue B

FIGURE 3.17  Dermatomyositis in a South American woman (heliotrope rash) (A). Dermoscopy: sparse white scaling and purplish background with follicular sparing, giving rise to a reticular aspect (B).

A

B

FIGURE 3.18  Back involvement in the patient shown in the previous image (A). Dermoscopy: purplish background with perifollicular white areas (B).

A

B

FIGURE 3.19  Dermatomyositis involving the face in an Indian woman (A). Dermoscopy: diffuse brown background with white perifollicular areas; subtle linear vessels are also evident (B).

45

Dermoscopy for skin of colour A

B

FIGURE 3.20  Dermatomyositis involving the dorsal aspect of the hands in a Caribbean woman (A). Dermoscopy of the proximal nailfold reveals elongated and dilated capillaries and a hyperkeratotic cuticle (B).

A

B

FIGURE 3.21  Hypertrophic proximal nailfold in an Indian patient suffering from dermatomyositis (A). Dermoscopy: hyperkeratotic cuticle along with focal white structureless areas and brown pigmentation (B).

3.7  Morphea and systemic sclerosis 3.7.1 Introduction Morphea and systemic sclerosis (SSc) are two autoimmune connective tissue diseases typified by excessive collagen deposition, with consequent thickening and hardening of the dermis and/or subcutaneous tissues.14,17 Although the former is typically limited to the skin, the latter also involves visceral organs.14,17 Additionally, differently from SSc, morphea classically does not show sclerodactyly, Raynaud phenomenon, proximal nailfold capillary abnormalities and telangiectasias.14,17 Compared with Caucasians, African Americans have a greater age-specific incidence of SSc, with an earlier age of onset and disease severity, whereas morphea is more common in fair-skinned patients.14,17

3.7.2  Clinical presentation Morphea classically presents with one or more inflammatory, oedematous, reddish to greyish/brownish (especially in darker phototypes) circumscribed patches, which then develop a central sclerosis manifesting as thickening and ivory white discolouration usually devoid of hair follicles (Figures 3.22A and 3.23A).14,17 A reddish/greyish-brownish border (lilac ring) around the sclerotic area is usually seen in active lesions.14,17 Over time, the sclerotic patches may soften and become atrophic with hypopigmentation or hyperpigmentation.14,17 Morphea encompasses several less common morphological variants, including guttate, keloidal/nodular, bullous, linear (Figure 3.24A), generalized, deep and pansclerotic subtype.14,17 SSc lesions begin symmetrically on the fingers, with swelling of the fingers evolving into sclerosis with ulcerations and decreased ability to move the skin.14,17 Cutaneous involvement may progress following a proximal direction, with a

46 variable extension (Figure 3.25A).14,17 Skin manifestations are typically preceded/accompanied by Raynaud phenomenon and proximal nailfold capillary abnormalities.14,17 Areas of depigmentation sparing the perifollicular skin, resulting in a salt-and-pepper appearance, are particularly evident in darkskinned patients.14,17

3.7.3 Dermoscopy The dermoscopic hallmark of morphea in skin of colour is represented by focal (more common) or diffuse dull white areas having ill-defined margins (also called “white clouds” and “white fibrotic beams”) that histologically correspond to fibrosis in the deep dermis (Figures  3.22B–3.24B).7,14 Such structures are obviously seen in clinically sclerotic lesions, but also when sclerosis is not clearly visible on macroscopic examination.7,18 Notably, the presence of dull white areas, along with the absence of follicular plugs, is significantly

A

Granulomatous and connective tissue suggestive of morphea compared with extra-genital lichen sclerosus.7,18 Unlike in Caucasians, vessels are usually difficult to see, whereas it is possible to appreciate pigmentary structures, such as brown dots (resulting from dermal pigment incontinence) and brown structureless areas/lines (due to basal layer pigmentation) (Figures  3.22B and 3.23B).7,18 Additional dermoscopic features include patchy brown/white scales (related to hyperkeratosis), perifollicular white areas (due to selective perifollicular fibrosis), white lines (localized dermal fibrosis) (Figure  3.23B) and focal/diffuse bright white areas (corresponding to superficial fibrosis – rarer in morphea).7,18 SSc typically shows the same pattern as morphea, even though, in the former, the shade of white is often variable in the context of the lesion (probably due to a different deepness of fibrosis) and intermingled brownish structureless areas are far more common, especially perifollicular pigmentation (related to perifollicular sparing) (Figure 3.25B).14

B

FIGURE 3.22  Morphea of the abdomen in an Indian man (A). Dermoscopy: ill-defined multifocal dull white areas (B).

A

B

FIGURE 3.23  Diffuse morphea of the abdomen in an Indian man (A). Dermoscopy: ill-defined multifocal dull white areas along with bright white lines (B).

47

Dermoscopy for skin of colour A

B

FIGURE 3.24  Linear morphea of the forehead in an Indian girl (A). Dermoscopic examination shows ill-defined dull white areas disrupting the physiological brown pseudonetwork (B).

A

B

FIGURE 3.25  Systemic sclerosis in an Indian woman (A). Dermoscopy reveals white areas displaying a variable shade and intermingled brownish structureless areas (B).

3.8  Lichen sclerosus 3.8.1 Introduction Lichen sclerosus is an autoimmune, chronic, scleroatrophic, inflammatory condition typically affecting the anogenital area (85% of cases), with extragenital (cutaneous) involvement occurring in a minority of cases (15%) (with or without anogenital lesions).14

3.8.2  Clinical presentation Lichen sclerosus presents as whitish, polygonal papules coalescing to form plaques of varying sizes and shapes (Figures  3.26A and 3.27A).14 Both anogenital and cutaneous lesions may also display fissures, telangiectasias, purpura, erythema and erosions.14 On the other hand, follicular plugs and scaling/hyperkeratosis are usually visible only in active

extragenital lesions.14 Over time, lesions become smooth and atrophic, with possible scarring sequelae on anogenital areas.14 In very dark phototypes, skin lesions may also be hyperpigmented (especially in the chronic phases), thus making diagnosis more difficult (Figure 3.28A).14 Unlike extragenital lesions, anogenital involvement is often symptomatic, with itching, soreness, dyspareunia, dysuria, discomfort with defecation and/or bleeding.14

3.8.3 Dermoscopy The dermoscopic aspect of lichen sclerosus varies according to the localization and clinicopathological stage (Figures 3.26B–3.28B).14,18 Bright white areas (focal or diffuse) and follicular plugs (white, yellow or brownish) are the main dermoscopic features of extragenital lesions (Figures  3.26B and 3.28B).7,14,18 They respectively correspond to homogenous fibrosis/hyalinization

48

Granulomatous and connective tissue A

B

FIGURE 3.26  Extragenital lichen sclerosus of the trunk in an Indian boy (A). Dermoscopy: bright white areas along with grey follicular plugs (B).

A

B

FIGURE 3.27  Genital lichen sclerosus in an African man (A). Bright structureless areas, linear bright lines and linear/serpiginous vessels are evident on dermoscopic assessment (B).

A

B

FIGURE 3.28  Extragenital lichen sclerosus of the back in a Caribbean woman (A). Dermoscopic examination displays perifollicular white areas as well as brown follicular plugs (B).

Dermoscopy for skin of colour of the superficial dermis and follicular plugs on histology.7,14,18 Additionally, white/brown scaling (due to hyperkeratosis), white perpendicular lines (due to dermal fibrosis), perifollicular white colour (due to perifollicular fibrosis), purpuric dots/ areas (dermal haemorrhages) and linear vessels with branches may also be seen (Figures  3.26B and 3.28B).7,14,18 Moreover, brown structureless areas (resulting from basal cell layer hyperpigmentation) and dots (due to dermal pigment incontinence) are further findings observed in skin of colour (Figure 3.28B), especially in long-standing lesions.7,14,18 When it comes to anogenital lesions, the dermoscopic hallmark is the presence of white bright areas, whereas follicular plugs are typically lacking because of the absence of follicles on mucosae (except for cutaneous areas of anogenital areas) (Figure  3.27B).14 Additional findings include purpuric spots (dots, globules, or structureless areas), pigmented dots/globules, erosions, scaling and vessels (dotted, linear, or linear curved/with branches) (Figure 3.27B).14

REFERENCES

1. Errichetti E, Lallas A. Granulomatous noninfectious disorders. In: Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press, 2018:56–64. 2. McKinley-Grant L, Warnick M, Singh S. Cutaneous manifestations of systemic diseases. In: Dermatology for Skin of Colour (Kelly AP, Taylor SC, eds), 1st edn. New York: McGraw-Hill Medical, 2009:489–510. 3. Jackson-Richards D. Sarcoidosis. In: Dermatology Atlas for Skin of Colour (Jackson-Richards D, Pandya AG, eds), 1st edn. Berlin: Springer-Verlag, 2014:141–5. 4. Errichetti E, Stinco G. Dermoscopy in general dermatology: A  practical overview. Dermatol Ther (Heidelb) 2016;6:471–507. 5. Errichetti E. Dermoscopy of inflammatory dermatoses (inflammoscopy): An up-to-date overview. Dermatol Pract Concept 2019;9:169–80. 6. Errichetti E, Stinco G. Dermatoscopy of granulomatous disorders. Dermatol Clin 2018;36:369–75.

49 7. Errichetti E, Ankad BS, Sonthalia S, et  al. Dermoscopy in general dermatology (non-neoplastic dermatoses) in skin of colour: A  comparative retrospective study by the International Dermoscopy Society. Eur J Dermatol 2020. doi: 10.1684/ejd.2020.3928 8. Yahya H. Necrobiosis lipoidica in a Nigerian woman: Report of a case. Niger J Clin Pract 2019;22:1626–8. 9. Mahmoud B, Jackson-Richards D. Granuloma annulare. In: Dermatology Atlas for Skin of Colour (Jackson-Richards D, Pandya AG, eds), 1st edn. Berlin: Springer-Verlag, 2014:147–9. 10. Errichetti E, Lallas A, Apalla Z, Di Stefani A, Stinco G. Dermoscopy of granuloma annulare: A clinical and histological correlation study. Dermatology 2017;233:74–9. 11. Rocos D, Kanitakis J. Lupus miliaris disseminatus faciei: Report of a new case and brief review of literature. Dermatol Online J 2013;19:4. 12. Chauhan P, Jindal R, Shirazi N. Dermoscopy of lupus miliaris disseminatus faciei: A  step closer to diagnosis. Dermatol Pract Concept 2020;10:e2020055. 13. Chauhan P, Adya KA. Dermatoscopy of cutaneous granulomatous disorders. Indian Dermatol Online J 2021;12:34–44. 14. Errichetti E, Lallas A. Connective tissue diseases. In: Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press, 2018:65–85. 15. Grabell D, Bowman KA, Chong BF. Cutaneous lupus erythematosus. In: Dermatology Atlas for Skin of Colour (Jackson-Richards D, Pandya AG, eds), 1st edn. Berlin: Springer-Verlag, 2014:153–9. 16. Bowman KA, Chong BF. Dermatomyositis. Cutaneous lupus erythematosus. In: Dermatology Atlas for Skin of Colour (Jackson-Richards D, Pandya AG, eds), 1st edn. Berlin: Springer-Verlag, 2014:161–6. 17. Baker LA, Jacobe HT. Scleroderma and morphea. In: Dermatology Atlas for Skin of Colour (Jackson-Richards D, Pandya AG, eds), 1st edn. Berlin: Springer-Verlag, 2014:167–73. 18. Errichetti E, Lallas A, Apalla Z, Di Stefani A, Stinco G. Dermoscopy of morphea and cutaneous lichen sclerosus: Clinicopathological correlation study and comparative analysis. Dermatology 2017;233:462–70.

4 Facial inflammatory dermatoses

Facial inflammatory dermatoses

Dermoscopy for skin of colour

Enzo Errichetti, Feroze Kaliyadan, Jayasree Puravoor, Balachandra Ankad, Bengu Nisa Akay and Aimilios Lallas

4.1  Acne vulgaris 4.1.1 Introduction Acne vulgaris is an inflammatory disorder of the pilosebaceous unit typical of adolescent age, even though adulthood onset is not rare in females.1,2 It is a multifactorial condition related to an increased sebum production, keratinocyte hyperproliferation, inflammation and altered bacterial colonization, especially by Propionibacterium acnes.1,2 Such a disorder seems to be quite common in dark-skinned patients.1

4.1.2  Clinical presentation Lesions typical of acne (Figure 4.1A) include comedones (both closed comedones, appearing as a small whitish/skin-coloured papule, and open comedones, presenting as a blackish spot corresponding to a pilosebaceous orifice filled with keratin, skin debris and sebum), inflammatory papules, pustules, nodules and cysts.1,2 The face is the most common involved site, followed by the upper chest and upper back.1,2 Acneiform eruptions are the main differential diagnosis of acne vulgaris (Figure 4.2A).1,2 Notably, postinflammatory hyperpigmented macules are extremely common in darker-skinned individuals, whereas

A

nodulocystic presentations tend to be less common in the African American population, but when nodules and cysts occur, they often result in hypertrophic scarring and keloids.1 Nodulocystic acne may sometimes be part of the so-called “follicular occlusion syndrome”, along with hidradenitis suppurativa and dissecting cellulitis (Figure  4.3A) (“follicular occlusion triad”).1,2

4.1.3 Dermoscopy Apart from inflammatory lesions (i.e., papules, pustules and cysts), dermoscopic examination allows the hallmark of acne vulgaris lesions, namely comedones, to be seen.2 In particular, closed comedones appear as skin-coloured or white areas, whereas open comedones present as dilated pores filled with brownish/greyish keratin (Figure  4.1B).2 The evidence of comedones (especially open subtypes) may come in handy to differentiate acne vulgaris from acneiform eruptions (e.g., drug-induced forms) as the latter typically do not display such a feature (Figure  4.2B).2 Notably, open comedones are also seen in hidradenitis suppurativa and dissecting cellulitis (even in the early phases) thereby supporting a prompt diagnosis of such disorders.2

B

FIGURE 4.1  Acne vulgaris in an African boy (A). Dermoscopy reveals closed comedones, appearing as skin-coloured/white round areas (arrowhead), and open comedones, presenting as dilated pores filled with brownish/greyish keratin (arrows) (B).

DOI: 10.1201/9780367816483-4

52

Facial inflammatory dermatoses A

B

FIGURE 4.2  Medication-associated acneiform eruption in an Indian boy (A). Dermoscopic examination shows several yellow pustules with no closed/open comedones (B).

A

B

FIGURE 4.3  Erythematotelangiectatic rosacea in a Caribbean woman (A). Dermoscopy shows blurred linear vessels arranged in a reticular pattern (the so-called “vascular polygons”) and periostial brown circles (B).

4.2 Rosacea 4.2.1 Introduction Rosacea is a benign, inflammatory dermatosis, mainly affecting the central face, characterized by abnormal vasomotor responses, persistent vasodilatation and increased vascular permeability.2,3 Bacillus oleronius (a bacterium isolated from Demodex folliculorum) is thought to act as a trigger for a susceptible innate immune system in rosacea patients.2,3 Even though it is most frequent in light-skinned patients, rosacea may also occur in darker phototypes.2,3

4.2.2  Clinical presentation There are three main forms of rosacea: erythematotelangiectatic, papulopustular and glandular variants.2,3 Erythematotelangiectatic rosacea manifests as transient burning flushing involving the centrofacial areas as a response to several stimuli (e.g., temperature changes, specific foods, or stress), followed by permanent erythema associated with telangiectatic vessels (poorly visible in darker phototypes)

(Figure  4.3A).2,3 On the other hand, papules and pustules on an erythematous background are typical of the papulopustular variant, whereas disfiguring skin enlargements belong to the glandular form (e.g., rinophyma) (Figure  4.4A).2,3 Granulomatous and ocular rosacea are other less common variants.2,3

4.2.3 Dermoscopy The dermoscopic hallmark of erythematotelangiectatic rosacea is represented by blurred linear vessels arranged in a reticular pattern (the so-called “vascular polygons”) (Figure 4.3B), histologically corresponding to dilated blood vessels in reticular dermis.4–6 Unlike in Caucasians, in darker phototypes, the pigmentary structures are common, including periostial brown globules and periostial brown circles (Figure 4.3B).4–6 In papulopustular rosacea, dermoscopy facilitates the visualization of pustules, along with the previously mentioned vascular pattern, whereas dilated follicular openings filled with sebum are typically seen on dermoscopic examination of glandular rosacea (Figure 4.4B).4–6 Finally, granulomatous rosacea is characterized by orange-coloured areas, histologically corresponding to granulomas, as well as vascular polygons.4–6,7

53

Dermoscopy for skin of colour A

B

FIGURE 4.4  Glandular rosacea in a man from the Middle East (A). Dermoscopic examination displays a pustule, vascular polygons, pigmentation around the facial ostia and dilated follicular openings filled with sebum (arrows) (B).

4.3  Seborrheic dermatitis 4.3.1 Introduction Seborrheic dermatitis (SD) is a frequent inflammatory skin disorder involving areas characterized by high sebum production.2,8 Sebum composition-related factors and an individual’s immune response to Malassezia seem to play a pathogenetic role.2,8 Two main forms do exist, a self-limiting infantile form (from birth to 3 months of age) and a chronic/relapsing adult form (peaking at ages 30–60).2,8

4.3.2  Clinical presentation Infantile SD typically presents as yellowish, greasy scale on the scalp that is often referred to as “cradle cap”.2,8 Additionally, erythematous patches, with or without yellowish/ greyish scales, may also be seen in other districts, such as the face, retroauricular area, axillae and inguinal folds.2,8 On the other hand, the adult form presents with erythema and scaling (yellowish/greyish greasy scales) symmetrically affecting the nasolabial folds (Figure 4.5A), malar areas, glabella and eyebrows.2,8 Other commonly involved areas are the beard area (Figure 4.6A), external ear, retroauricular area and presternal area.2,8 Postinflammatory hypopigmented patches are quite common in dark-skinned patients (Figure 4.7A).2,8

4.3.3 Dermoscopy Dermoscopic examination of SD displays clustered vessels (especially dotted but also linear) along with patchy scales, whose colour may be white (hyperkeratosis), yellow (hyperkeratosis + serum due to spongiosis), or brown (hyperkeratosis + exfoliated melanin) (Figures  4.5–4.7B).4–6 Notably, vessels are difficult to see in darker phototypes.4–6 Additionally, unlike Caucasian patients, in dark-skinned subjects, it is also quite common to see white structureless areas (Figures 4.6B and 4.7B), resulting from postinflammatory hypopigmentation, and whitish/yellowish, protruding/non-protruding, broad

follicular plugs (“sebum excrescences” due to sebum and keratin accumulation in follicles) (Figure  4.5B).4–6 These latter structures should be distinguished from the protruding follicular plugs seen in demodicosis (resulting from mites and keratin deposits in the follicles), which are typically white as well as thinner and longer compared with “sebum excrescences” visible in facial SD in skin of colour.4–6

4.4 Pseudofolliculitis 4.4.1 Introduction Pseudofolliculitis is a chronic inflammatory disorder secondary to aberrant hair growth in areas where the hair is shaved.8–10 It is considered a foreign body type reaction secondary to intraepidermal, transepidermal or transfollicular penetration of the sharp, free hair shaft ends after shaving.8–10

4.4.2  Clinical presentation Pseudofolliculitis is more common in people with curly hair (which increases the chance of aberrant hair entry).8–10 Patients classically present with acneiform papules in areas of shaving, often causing mild pruritus (Figure 4.8A).8–10 Secondary infection can be associated with pustules and, more uncommonly, abscesses, cysts and keloidal scars.8–10

4.4.3 Dermoscopy The most characteristic feature visible on dermoscopic examination is represented by the “handlebar sign”, which corresponds to the ingrown hair, apparently attached at both ends (Figure 4.8B).8,10 Other signs of inflammation seen include yellow areas, correlating with pustule/abscess formation, scales, surrounding erythema and vessels (which may be dotted and/or irregular linear).8,10 Partially or completely buried hair shafts dermoscopically appearing like bluish lines (Figure 4.8B) are another helpful clue in the diagnosis of pseudofolliculitis.8,10

54

Facial inflammatory dermatoses B

A

FIGURE 4.5  Seborrheic dermatitis in an Indian man (A). Dermoscopy reveals patchy white/yellow scales along with protruding, broad follicular plugs (“sebum excrescences” due to sebum and keratin accumulation in the follicles – arrows) (B). (Courtesy of Soumil Khare, MD – Raipur, India.)

A

B

FIGURE 4.6  Seborrheic dermatitis of the face in an Indian boy (A). Dermoscopy: patchy brown scales and focal dull white structureless areas (B).

A

B

FIGURE 4.7  Seborrheic dermatitis of the face in an African woman (A). Dermoscopy: focal dull white structureless areas disrupting the physiological pigmentation of the face (B).

55

Dermoscopy for skin of colour A

B

FIGURE 4.8  Pseudofolliculitis over the beard area in an Indian man (A). Dermoscopic assessment reveals partially and completely ingrown hair shafts, white areas corresponding to fibrosis and a hair apparently attached at both ends (handlebar sign – arrow) (B).

4.5  Granuloma faciale 4.5.1 Introduction Granuloma faciale (GF) is an uncommon and benign skin condition of unknown aetiology that is histologically typified by a chronic leukocytoclastic vasculitis with fibrosing evolution.2 Such a disorder tends to occur in middle-aged white patients, yet it has been reported also in dark-skinned subjects.2

4.5.2  Clinical presentation From a clinical point of view, GF in skin of colour manifests as one or, more frequently, multiple reddish-brownish or purple-brownish papules, nodules or plaques over the face (Figure  4.9A), although extra-facial locations are possible.2 Prominent follicular orifices (peau d’orange) may be seen on the facial lesion’s surface.2 GF is usually asymptomatic, yet pruritus and pain may be present.2

A

4.5.3 Dermoscopy Dermoscopic examination of GF is poorly studied in darkskinned patients. The most common and relevant dermoscopic feature is represented by prominent follicular orifices (Figure 4.9B) possibly related to an in vivo phenomenon likely because of an inflammation sparing of the superficial dermis (“narrow grenz zone”) with consequent laxity of the follicular ostia.4,5 Other dermoscopic features include linear branching vessels (difficult to see in darker phototypes), whitish halo, pigmentation structures (especially in darker phototypes  – authors’ personal observations) (Figure 4.9B), follicular plugs, yellowish scales, whitish streaks and whitish-greyish structureless areas, with the last two findings being more common in long-standing lesions characterized by dermal fibrosis.4,5 Additionally, purpuric spots (histologically corresponding to erythrocytes extravasation) may also be seen in early lesions, with subsequent appearance of orangish areas (resulting from dermal hemosiderin deposits).4,5

B

FIGURE 4.9  Granuloma faciale in an Asian man (A). Dermoscopy shows a brownish background and dilated follicular openings (arrows); blurred linear vessels are also seen at the periphery (B).

56

Facial inflammatory dermatoses

REFERENCES









1. Jackson-Richards D. Acne vulgaris. In: Dermatology Atlas for Skin of Colour (Jackson-Richards D, Pandya AG, eds), 1st edn. Berlin: Springer-Verlag, 2014:101–8. 2. Errichetti E, Kaliyadan F, Lacarrubba F, Verzì AE, Micali G, Lallas A. Facial dermatoses. In: Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press, 2018:86–96. 3. Isedeh P, Jackson-Richards D. Rosacea. In: Dermatology Atlas for Skin of Colour (Jackson-Richards D, Pandya AG, eds), 1st edn. Berlin: Springer-Verlag, 2014:73–6. 4. Errichetti E, Stinco G. Dermoscopy in general dermatology: A  practical overview. Dermatol Ther (Heidelb) 2016;6:471–507. 5. Errichetti E. Dermoscopy of inflammatory dermatoses (inflammoscopy): An up-to-date overview. Dermatol Pract Concept 2019;9:169–80.

6. Errichetti E, Ankad BS, Sonthalia S, et  al. Dermoscopy in general dermatology (non-neoplastic dermatoses) in skin of colour: A  comparative retrospective study by the International Dermoscopy Society. Eur J Dermatol 2020. doi: 10.1684/ejd.2020.3928 7. Jackson-Richards D. Seborrheic dermatitis. In: Dermatology Atlas for Skin of Colour (Jackson-Richards D, Pandya AG, eds), 1st edn. Berlin: Springer-Verlag, 2014:109–14. 8. Kaliyadan F, Kuruvilla J, Al Ojail HY, Quadri SA. Clinical and dermoscopic study of pseudofolliculitis of the beard area. Int J Trichology 2016;8:40–2. 9. Panchaprateep R, Tanus A, Tosti A. Clinical, dermoscopic, and histopathologic features of body hair disorders. J Am Acad Dermatol 2015;72:890–900. 10. Ladizinski B, Ramirez-Fort MK, Cohen YK, Rosendahl C, Elpern DJ. Pseudofolliculitis barbae: A dermatoscopic correlate. Dermatol Pract Concept 2013;3:53–4.

5 Hyperpigmented dermatoses

Hyperpigmented dermatoses

Dermoscopy for skin of colour

Shekhar Neema

5.1  Lichen planus pigmentosus

5.1.3 Dermoscopy

5.1.1 Introduction

Dermoscopic examination of LPP involving the face mainly shows pigmented dots typically arranged around follicular and eccrine ostia (“periostial arrangement”) (Figure  5.1B).5–7 Importantly, the dots may be brown or grey, yet only the former has been found to be significantly associated with the LPP diagnosis compared with other main pigmented facial diseases (i.e., ashy dermatosis, Riehl melanosis, melasma, exogenous ochronosis and nevus of Ota).5–7 Focal brown structureless areas with ostial sparing are also visible.5–7 On extra-facial areas, brown dots over a brown background represent the main dermoscopic feature of LPP (Figures  5.2B and 5.3B); additional findings include grey dots as well as brown and grey dots.5–7 From a dermoscopic-pathological point of view, pigmented dots, globules and structureless areas correspond to pigment incontinence (as free melanin or melanophages) in the papillary dermis (brown structures) or upper reticular dermis (grey structures) resulting from dermoepidermal junction damage caused by the peculiar lichenoid inflammation located just below the epidermis.5–7

Lichen planus pigmentosus (LPP) is an uncommon variant of lichen planus that is mainly seen in Indian patients but also occurs not rarely in Latin Americans and very darkly pigmented subjects.1–4

5.1.2  Clinical presentation LPP is clinically characterized by asymptomatic, brownish/ greyish macules/patches mainly distributed on sun-exposed areas (e.g., the face and neck) (Figure  5.1A) or flexural skin (e.g., axillae and inguinal areas) (Figure 5.2A).1–4 Several morphological variants have been described, mainly including diffuse (Figure 5.3A), reticular, linear, blotchy, perifollicular and annular.1–4

A

B

FIGURE 5.1  Lichen pigmentosus of the beard area in a North African man (A). Dermoscopy reveals brown dots around the follicles (B). (Panel B from Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press.)

DOI: 10.1201/9780367816483-5

58

Hyperpigmented dermatoses

A

B

FIGURE 5.2  Lichen pigmentosus of the abdomen in an African woman (A). Dermoscopic examination shows brown dots over a brown background (B). (Courtesy of Enzo Errichetti, MD – Udine, Italy.)

A

B

FIGURE 5.3  Diffuse lichen pigmentosus in an Indian man (A). Dermoscopy: brown-grey dots around the follicular openings giving rise to a reticular pattern (B).

5.2  Ashy dermatosis 5.2.1 Introduction Ashy dermatosis (also known as erythema dyschromicum perstans) is a slowly progressive pigmentary skin condition mainly affecting young adults.4,8 It is regarded as an idiopathic condition, yet a response to antigenic stimulation might play a role in its etiopathogenesis.4,8

5.2.2  Clinical presentation Ashy dermatosis typically manifests as grey to blue macules/ patches symmetrically distributed over the trunk (Figure 5.4A), although it may also involve the face, neck (Figure 5.5A), upper limbs and, less frequently, lower limbs.4,8 A slightly raised erythematous border or hypopigmented macules/areas (Figure 5.6A) may also be seen in a minority of cases.4,8 Lesions are usually asymptomatic, yet a moderate pruritus may be present.4,8

59

Dermoscopy for skin of colour

5.2.3 Dermoscopy The main dermoscopic feature of ashy dermatosis (including both pigmented and hypopigmented lesions) is represented by the presence of grey and blue dots (Figures 5.4–5.6), with the latter being more frequent.6,7 Histologically, these dermoscopic structures are related to the presence of melanophages/ A

melanin deposits in superficial (grey dots) or deep (blue dots) reticular dermis.6,7 Notably, on the face, the dots are distributed in a periostial pattern (similarly to lichen planus pigmentosus).6,7 Additional relevant dermoscopic findings of the face and extra-facial areas include grey/blue globules (with a periostial arrangement on the face) and a bluish background (with an ostial sparing on the face).6,7,8 B

FIGURE 5.4  Ashy dermatosis on the back of an Indian girl (A). Dermoscopy: small grey-blue dots over a bluish background (B). (Courtesy of Enzo Errichetti, MD – Udine, Italy.)

A

B

FIGURE 5.5  Diffuse ashy dermatosis in an Indian man (A). Dermoscopic assessment displays perifollicular grey-blue dots (B).

A

B

FIGURE 5.6  Ashy dermatosis with both hyperpigmented and hypopigmented patches (A). Dermoscopy reveals bluish dots over a whitish background (B). (Courtesy of Enzo Errichetti, MD – Udine, Italy.)

60

5.3  Dowling-Degos disease 5.3.1 Introduction Dowling-Degos disease (DDD) is an autosomal dominant genodermatosis with variable penetrance typically arising during adulthood.9,10 It is due to loss of function mutations in the keratin 5 gene, protein O-fucosyltransferase 1 (POFUT1) and protein O-glucosyltransferase 1 (POGLUT1).9,10

5.3.2  Clinical presentation DDD manifests as brown macules arranged in a reticular pattern classically involving the flexures (Figure  5.7A).9,10 Additionally, pitted perioral scars, palmoplantar pits and follicular hyperkeratotic papules are present (Figure  5.7B).9,10 Possible variants/related conditions include follicular DDD, A

Hyperpigmented dermatoses generalized DDD, Galli-Galli disease, Haber’s syndrome, reticulate acropigmentation of Kitamura, reticulate acropigmentation of Dohi and pigmentatio reticularis faciei et colli.9,10

5.3.3 Dermoscopy Dermoscopy of hyperpigmented macules of DDD in skin of colour reveals a central hypopigmented area (corresponding to follicular infundibulum) with surrounding irregular brownish projections or accentuated reticular pigment pattern (elongated rete ridges with pigmentation at the tips) (Figure 5.8A), whereas hypopigmented lesions feature a white area with perifollicular pigment retention and surrounding accentuation of a reticular pigment pattern (Figure  5.8B).11,12 Finally, keratin plugging with breaks in the dermatoglyphics by linear pigmented furrows may be observed on dermoscopic assessment of palmar pits.11,12 B

FIGURE 5.7  Clinical image of Dowling-Degos disease in an Indian woman shows hyperpigmented macules involving the upper arm (A) and pitted perioral scars (B).

A

B

FIGURE 5.8  Dowling-Degos disease. Dermoscopy: hyperpigmented macule shows periostial hypopigmentation and an accentuated reticular pigment network (better seen in the inset) (A), whereas the hypopigmented macule displays a depigmented centre and an accentuated reticular network and periosteal pigmentation at the periphery (better seen in the inset) (B).

61

Dermoscopy for skin of colour

5.4  Macular amyloidosis and lichen amyloidosis 5.4.1 Introduction Macular amyloidosis and lichen amyloidosis are the main forms of primary cutaneous amyloidosis, histologically characterized by deposition of amyloid in the papillary dermis in previously healthy skin without any internal organ deposition.13,14

5.4.2  Clinical presentation Macular amyloidosis presents as areas of rippled pigmentation mainly involving the upper back or extensor aspects of the limbs (Figure 5.9A), whereas lichen amyloidosis is typified by itchy dome-shaped brown papules more commonly affecting the legs (Figure  5.10A).13,14 Overlapping cases (“biphasic” or “mixed” amyloidosis) may be observed.13,14

A

5.4.3 Dermoscopy Dermoscopy of macular amyloidosis and lichen amyloidosis in dark-skinned patients typically reveals an overlap, with a central brown or white dot/globule with peripheral pigmentation (usually radiating brown streaks, but also brown dots) being the most characterizing pattern of both such conditions (Figures  5.9B and 5.10B).6,13,14 These dermoscopic features result from roundish amyloid deposits – with or without melanin  – in the tips of dermal papillae (central dot/globule) and adjacent basal layer pigmentation or dermal free melanin/ melanophages (peripheral pigmentation).6,13,14 Notably, in very dark phototypes, peripheral pigmentation may not be clearly visible on dermoscopy.6,14 Further (unspecific) dermoscopic findings seen in both the conditions include structureless white or brown areas and brown dots/globules (Figures  5.9B and 5.10B).6,13,14 Additionally, white scales (central or patchy) and broken hairs may also be observed in lichen amyloidosis.6,13,14

B

FIGURE 5.9  Macular amyloidosis of the back in an Indian man (A). Dermoscopy: diffuse brown dots and multifocal brown structureless pigmentation along with the characteristic structures consisting of central white globules with peripheral pigmentation (in this case mainly brown dots) (arrows) (B).

A

B

FIGURE 5.10  Lichen amyloidosis in an Indian man (A). Dermoscopy: several papules display central brown dots with peripheral pigmentation (in this case mainly radial brown striae) (arrows); some lesions also display a white halo (B).

62

Hyperpigmented dermatoses

5.5  Friction melanosis 5.5.1 Introduction Friction melanosis is an acquired hyperpigmented dermatosis due to repeated and persistent skin rubbing, which is thought to be the result of melanosomes squeezing into the dermis and their further engulfment by the macrophages.15 It is typically more frequent in skin of colour.15

5.5.2  Clinical presentation It manifests as either diffuse or mottled brown patches most commonly involving the bony prominences, such as the clavicular zone and upper back (Figure 5.11A), but also the face may be affected in dark-skinned patients (Figure 5.12A).15 The main clinical differential diagnosis is macular amyloidosis (extra-facial lesions).15

A

5.5.3 Dermoscopy The typical dermoscopic pattern of friction melanosis in skin of colour consists of a structureless brown area and/or reticular brown network (histologically corresponding to basal layer hyperpigmentation) along with perifollicular hypopigmentation (corresponding to scratching-induced perifollicular acanthosis) (Figure 5.11B).6,16 Of note, this last finding is typical of darker phototypes probably because of a higher tendency to follicular reactions in ethnic skin.6,16 Additional less common dermoscopic findings include focal white areas, brown dots/ globules and white globules.6,16 Friction melanosis of the face typically displays an accentuation of the brown pseudonetwork (structureless brown areas with ostial sparing), with or without periostial pigmentation (brown circles) (Figure 5.12B).6

B

FIGURE 5.11  Friction melanosis involving the back of an African woman (A). Dermoscopy reveals multifocal brown structureless areas along with perifollicular hypopigmentation (arrow) (B). (Courtesy of Enzo Errichetti, MD – Udine, Italy.)

A

B

FIGURE 5.12  Friction melanosis of the face in an Indian man (A). Dermoscopic examination displays an accentuation of a brown pseudonetwork (structureless brown areas with ostial sparing) and periostial pigmentation (arrows) (B). (Courtesy of Balachandra Ankad, MD – Bagalkot, India.)

63

Dermoscopy for skin of colour

5.6  Terra firma-forme dermatosis

5.7  Dermatosis neglecta

5.6.1 Introduction

5.7.1 Introduction

Terra firma-forme dermatosis (TFFD) is an acquired and idiopathic condition related to a delayed keratinocyte maturation, resulting into a retention of keratinocytes/melanin within the epidermis.17,18

Dermatosis neglecta results from a progressive accumulation of sebum, sweat, keratin, dirt and debris related to voluntary or unconscious inadequate cleansing of the skin.18 The lesions are routinely amenable to removal by washing with soap and water, differentiating it from TFFD.18

5.6.2  Clinical presentation

5.7.2  Clinical presentation

TFFD is typified by asymptomatic brown to black plaques resembling dirty skin, which disappear after rubbing with alcohol (but not with ordinary cleansing) (Figure 5.13A); the face, neck and trunk are the most commonly involved areas.17,18 It is often mistaken for dermatosis neglecta.17,18

It manifests as localized brownish patches or verrucous plaques whose surfaces may show adherent flaking scales (Figure 5.14A); the trunk and flexures are the most commonly involved areas.18

5.7.3 Dermoscopy

5.6.3 Dermoscopy The typical dermoscopic pattern of TFFD consists of large polygonal plate-like brown scales arranged in a regular mosaic pattern (Figure 5.13B) resulting from compact orthohyperkeratosis, acanthosis and papillomatosis; the brown colour of the scales is related to melanin exfoliation.18 A

From a dermoscopic point of view, dermatosis neglecta is classically characterized by irregularly distributed “cornflakelike” dark brown scales (Figure 5.14B) histologically related to prominent basket-weave hyperkeratosis as well as epidermal atrophy and diminution of rete pegs (responsible for a more irregular pattern compared with TFFD).18

B

FIGURE 5.13  Terra firma-forme dermatosis in a Filipino woman (A). Large polygonal plate-like brown scales arranged in a regular mosaic pattern are visible on dermoscopy (B). (Courtesy of Enzo Errichetti, MD – Udine, Italy.)

A

B

FIGURE 5.14  Dermatosis neglecta in an Indian boy (A). Dermoscopic assessment displays irregularly distributed “cornflake-like” dark brown scales (B).

64

Hyperpigmented dermatoses

5.8 Melasma 5.8.1 Introduction Melasma is a common pigmentary disorder typically affecting sun-exposed areas with a multifactorial and complex pathogenesis in which are involved both a genetic predisposition and acquired factors (e.g., sun exposure, hormonal factors and medications).19 It is much more common in skin of colour.19

5.8.2  Clinical presentation Melasma presents as symmetrical hyperpigmented (brownish to greyish) macules and patches classically involving the face, particularly the malar areas and forehead (Figure 5.15A), yet extra-facial sites (e.g., the trunk and forearms) may rarely be affected.19 Two main clinic-pathological variants do exist, i.e., epidermal and dermal melasma, respectively characterized by sharp and ill-defined margins; Wood’s lamp may help analyse lesion borders.19 Mixed forms are possible.19

5.8.3 Dermoscopy Dermoscopy helps in the diagnosis of melasma and its differentiation from other facial melanosis, treatment monitoring

A

and treatment-associated side effects, such as exogenous ochronosis and steroid-induced telangiectasias.6,20,21 The main dermoscopic pattern of facial melasma is represented by brown structureless areas with ostial sparing (pseudonetwork) having a focal/multifocal or, most commonly, a diffuse (as a background) (Figure  5.15B) distribution histologically related to basal layer hyperpigmentation.6,20,21 Focal grey structureless areas with ostial sparing and interostial brown/grey dots may also be seen and may be related to a dermal pigment component (“dermal melasma”).6,20,21 Periostial (follicles/eccrine sweat glands) brown pigmentation (periostial brown circles) may also be seen in a minority of cases (Figure 5.16A).6,20,21 Finally, telangiectasias (blurred linear-branching/reticular vessels) (Figure  5.16B) may also be visible as a primary vascular component or as a result of steroid overuse.6,20,21 This may affect the treatment choice as the presence of a significant vascular component on dermoscopic assessment (“telangiectatic melasma”) would support the use of a laser therapy targeting the vessels (e.g., pulseddye laser).6,20–22 Dermoscopy may also be useful in following up lesion changes during the treatment to see the attenuation/regression of pigmentary and vascular structures as well as in predicting therapeutic response in melasma as it may help assess lesion depth.6,20–22

B

FIGURE 5.15  Facial melasma in an Indian woman (A). Dermoscopy shows diffuse brown pigmentation with ostial sparing (brown pseudonetwork); a sparing of the skin furrows is also visible (B).

A

B

FIGURE 5.16  Dermoscopy of facial melasma: Brown pseudonetwork along with periostial brown and grey (because of a dermal component) pigmentation (A); accentuation of the brown network is associated with a vascular component (blurred linear-branching/reticular vessels) (B).

65

Dermoscopy for skin of colour

and 5.18A).23 The most common involved areas include the cheeks, temples and neck. Cases overlapping with melasma are possible (Figure 5.17A).23

5.9  Exogenous ochronosis 5.9.1 Introduction Exogenous ochronosis is a cutaneous pigmentary disorder primarily affecting dark-skinned individuals that is characterized by deposition of ochre-coloured pigment in the dermis.23 It is a complication of prolonged application of skin-lightening creams containing hydroquinone (especially for melasma), yet topical phenol or resorcinol and systemic antimalarials such as quinine are also implicated.23

5.9.2  Clinical presentation On clinical grounds, it is typified by asymptomatic blue-black skin macules or patches, which may feature sooty tipped papulations on the surface in more advanced phases (Figures 5.17A

A

5.9.3 Dermoscopy Focal white areas and interostial pigmentary structures (including brown/grey globules, circles and semicircles) (Figures 5.17B and 5.18B), respectively corresponding to focal loss of melanin and dermal ochre pigment arranged in different patterns on histology are the most characterizing dermoscopic features of facial exogenous ochronosis.6,24 Of note, such findings have been previously reported in the literature with the use of several “metaphoric” terms (“confetti-like” depigmentation, caviar-like structures, worm-like pattern, etc.).6,24 Additional possible dermoscopic findings (Figures 5.17B and 5.18B) include brown/grey structureless areas with ostial obliteration, pigmented interostial dots and fine telangiectasias.6,24

B

FIGURE 5.17  Exogenous ochronosis over a melasma background in an Indian woman (A). Dermoscopy: brown/grey pseudonetwork and periostial brown/grey pigmentation (epidermal/dermal melasma component) along with interostial brown-grey circles/semicircles (arrow in the inset) and focally distributed ostial obliteration (arrowheads) (exogenous ochronosis component) (B).

A

B

FIGURE 5.18  Exogenous ochronosis in an Indian woman (A). Dermoscopy reveals numerous interostial brown circles and semicircles (better visible in the inset) along with focal hypopigmented areas (B). (Courtesy of Vinay Keshavamurthy, MD – Chandigarh, India.)

66

Hyperpigmented dermatoses

5.10.3 Dermoscopy

5.10 Riehl melanosis (pigmented contact dermatitis) 5.10.1 Introduction Riehl melanosis, also known as pigmented contact dermatitis, is thought to be a non-eczematous variant of contact dermatitis characterized by skin pigmentary changes.25 It would result from a type 4 hypersensitivity reaction to the repeated contact with a low concentration of haptens, not enough to cause a spongiotic dermatitis but resulting in epidermal basal layer damage with consequent dermal pigment incontinence.25 It mainly occurs in dark phototypes.25

5.10.2  Clinical presentation Riehl melanosis manifests as a patchy or diffuse hyperpigmentation (brown, grey-brown or blue-brown) (Figures 5.19A and 5.20A) most commonly affecting the forehead and zygomatic and temporal areas, even though extra-facial involvement is also possible.25 A subtle erythema and pruritus may sometimes precede the pigmentary changes.25 A

The most common dermoscopic feature of facial Riehl melanosis in dark skin is represented by the presence of pigmented dots (Figure 5.19B), whose shade depends on the dermal pigment incontinence (free melanin/melanophages) depth.6 They are usually brown or grey, although blue dots may also be seen more rarely.6 The distribution of the dots may be perifollicular, interfollicular and intrafollicular (Figures  5.19B and 5.20B), with only the last arrangement pattern being specifically related to Riehl melanosis.6 Notably, intraostial dots are thought to be the result of an appendage reaction with pigment dispersion because of the possible trans appendage absorption of some haptens.6 Additional dermoscopic findings include telangiectasias, brown pseudonetwork (structureless areas with ostial sparing resulting from diffuse dermal pigment incontinence), sparse follicular keratotic plugs (due to follicular hyperkeratosis), perifollicular whitish halo (corresponding to perifollicular fibrosis) and white scales (representing epidermal hyperkeratosis) (Figures 5.19B and 5.20B).6

B

FIGURE 5.19  Riehl melanosis (pigmented contact dermatitis) of the face of an Indian woman (A). Dermoscopy: accentuation of pigmented pseudonetwork as well as brown pigmented dots mainly featuring interostial and intraostial (arrow) distribution (B).

A

B

FIGURE 5.20  Riehl melanosis (pigmented contact dermatitis) of the scalp of an Indian woman (A). Dermoscopy: grey diffuse pigmentation with ostial sparing (pseudonetwork) along with perifollicular white halos and grey dots featuring a periostial, interostial and intraostial (arrows) distribution (B).

67

Dermoscopy for skin of colour A

B

FIGURE 5.21  Erythema ab igne. Clinical image of erythema ab igne on the legs of a North African woman (A). Dermoscopic examination displays diffuse reddish-brownish discolouration with whitish scaling (B). (From Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press.)

5.11  Erythema ab igne

5.12  Pigmentary demarcation lines

5.11.1 Introduction

5.12.1 Introduction

Erythema ab igne is a benign condition characterized by a reticulated pattern of erythema and hyperpigmentation caused by repeated exposure to direct heat or infrared radiation, usually from occupational exposures or use of warm water bottles, heating pads and laptops.26

Pigmentary demarcation lines (PDL), also referred to as Futcher’s or Voight’s lines, are areas of abrupt transition between normal skin colour to darker colour seen over face, extremities and trunk in dark-skinned patients due to variable distribution of melanocytes.27

5.11.2  Clinical presentation It initially manifests with a temporary reticular erythema that is replaced by a fixed reticulated brown pigmentation as the exposure to heat continues over time (Figure 5.21A).26 Scaling or ulcerations may also be seen.26

5.11.3 Dermoscopy Dermoscopy in early lesions shows homogenous red-brown pigmentation surrounded by erythematous areas, whereas diffuse brownish pigmentation with telangiectasia and fine whitish scaling are visible in hyperpigmented lesions (Figure 5.21B).16

5.12.2  Clinical presentation Eight groups of PDL exist, including A–E, which are present over the trunk or extremities (Figure  5.22A), and F–H, localized over the face (Figure  5.23A).27 Facial PDL can be confused with melasma and postinflammatory pigmentation.27 Histopathology is non-specific with an increase in melanization.27

5.12.3 Dermoscopy Dermoscopy might show clear borders of abrupt transition between more and less pigmented skin areas and seen as an exaggerated or prominent reticular (Figure 5.22B) or pseudo-reticular (face) (Figure 5.23B) pattern (authors’ personal observations).

68

Hyperpigmented dermatoses A

B

FIGURE 5.22  Pigmentary demarcation line A (hyperpigmented area over the outer aspect of the upper arm) in an Indian girl (A). Dermoscopy shows clear demarcation between the involved and uninvolved areas and exaggerated reticular pigment network (B).

A

B

FIGURE 5.23  Pigmentary demarcation line G on the face (“W shaped” hyperpigmented area over the cheek) in an Indian girl (A). Dermoscopy displays an exaggerated pseudo-reticular pigment network (B).

5.13  Acanthosis nigricans 5.13.1 Introduction Acanthosis nigricans is a condition causing a dark cutaneous discolouration of the flexures that is frequently associated with obesity or diabetes.28 Further variants include unilateral, generalized, syndromic, malignant and medication-induced.28

5.13.2  Clinical presentation It is characterized by the presence of hyperpigmented coarse velvety plaques typically distributed symmetrically over the neck (Figure  5.24A), armpits and/or groins.28 Facial (Figure  5.25A) and acral lesions are also seen not rarely in

dark-skinned patients.28 Another ill-defined entity, “maturational hyperpigmentation”, can closely mimic facial acanthosis nigricans on clinical grounds.28

5.13.3 Dermoscopy Dermoscopy of acanthosis nigricans shows linear crista cutis and sulcus cutis (“sulci and gyri” pattern) (Figures 5.24B and 5.25B) or a “cobblestone” appearance, both of them resulting from papillomatosis and hyperpigmentation of the basal layer; hyperpigmented dots in the crista cutis, histologically corresponding to circumscribed basal layer hyperpigmentation over the tip of elongated dermal papillae, may also be seen.6 Dermoscopy of maturational hyperpigmentation shows brown rings and clods with perifollicular accentuation.6

69

Dermoscopy for skin of colour A

B

FIGURE 5.24  Acanthosis nigricans of the neck in an Indian woman (A). Dermoscopy shows linear crista cutis and sulcus cutis (“sulci and gyri” pattern).

A

B

FIGURE 5.25  Facial acanthosis nigricans in an Indian man (A). Even on the face, the dermoscopic examination shows a “sulci and gyri” pattern (B).

5.14  Postinflammatory hyperpigmentation 5.14.1 Introduction Postinflammatory hyperpigmentation (PIH) is an acquired hyperpigmentation secondary to any trauma/injury (chemicals, thermal) or inflammatory disorder (acne, lichen planus, etc.) of theskin.29 Dark-skinned individuals are prone to develop PIH owing to more epidermal melanin and production of melanin.29

5.14.2  Clinical presentation PIH is clinically typified by pigmented patches (Figure 5.26A) usually displaying various patterns of distribution depending

on the original dermatosis.29 The shade of the pigmentation varies from brown to grey/blue based on the histological background (brown due to basal layer pigmentation and grey/blue related to dermal pigment incontinence).29

5.14.3 Dermoscopy Dermoscopic assessment of PIH usually displays accentuation of the brown pseudonetwork (face) (Figure  5.26B) or reticular pigmentation (extra-facial sites) when there is basal layer hyperpigmentation on histology (the majority of cases), or brown, grey or bluish dots when the histological background is characterized by dermal pigment incontinence (e.g., lichen planus or discoid erythematous lupus).16 Mixed patterns may be observed.

70 A

Hyperpigmented dermatoses B

FIGURE 5.26  Postinflammatory hyperpigmentation following a minor trauma in an Indian boy (A). Dermoscopy shows brown coloured areas with ostial sparing (B).

A

B

FIGURE 5.27  Seborrheic melanosis showing hyperpigmentation involving the nasolabial fold in an Indian boy (A). Dermoscopy reveals a hyperpigmented pseudo-network and broad yellowish follicular plugs (“sebum excrescences” due to sebum and keratin accumulation in the follicles) (B).

5.15  Seborrheic melanosis 5.15.1 Introduction Seborrheic melanosis is considered a postinflammatory hyperpigmentation secondary to seborrheic dermatitis that is mainly seen in Asian, African and Hispanic populations.30

5.15.2  Clinical presentation From a clinical point of view, it manifests as localized darkening of seborrheic areas of the face (Figure  5.27A),

predominantly over the alar grooves, angles of the mouth and labio-mental crease.30

5.15.3 Dermoscopy Three categories of dermoscopic patterns have been reported, i.e., vascular, pigmented (the most common variant) and mixed pattern.31 In detail, the vascular pattern refers to arborizing and linear vessels over a light pink background, whereas the pigmented pattern is typified by a prominent hyperpigmented pseudo-network (Figure 5.27B).31 Protruding/non-protruding broad yellowish follicular plugs (“sebum excrescences”) due to sebum and keratin accumulation in the follicles may also be seen (Figure 5.27B).31

71

Dermoscopy for skin of colour

5.16  Gougerot-Carteaud syndrome 5.16.1 Introduction Gougerot-Carteaud syndrome (GCS), also known as confluent reticulated papillomatosis, is an uncommon but distinct dermatosis resulting from abnormal keratinocyte differentiation involving young adults; its pathogenesis is still poorly known, although several factors have been speculated to play a role, such as endocrine abnormalities (hyperthyroidism, diabetes and obesity), infections and a hereditary background.32,33

5.16.2  Clinical presentation GCS manifests as brown macules/slightly raised papules that coalesce to form plaques with peripheral reticulations (Figures 5.28A and 5.29A); white scaling or a verrucous surface may also be observed.32,33 It classically affects the upper trunk, neck and armpits, although abdominal and pubic area involvement may be seen.32,33

A

5.16.3 Dermoscopy Dermoscopy of GCS in skin of colour demonstrates white scales mainly arranged in the physiological skin furrows and perifollicular area, histologically corresponding to hyperkeratosis, and polygonal, flat, brown globules separated by whitish/pale striae creating a “cobblestone pattern” (“crocodile skin-like” appearance) (Figure 5.28B) or sulci and gyri giving rise to a “cerebriform pattern” (especially in thicker lesions) (Figure 5.29B).6,34,35 From a dermoscopic-pathologic point of view, the “cobblestone pattern” is related to basal layer hyperpigmentation, acanthosis and papillomatosis (resulting in brownish globules), with relative sparing of the normal network of furrows of the skin surface (representing the pale striae), whereas the “cerebriform pattern” results from basal layer hyperpigmentation along with the disruption of physiological grooves due to more pronounced/irregular acanthosis/ papillomatosis.6,34,35

B

FIGURE 5.28  Gougerot-Carteaud syndrome in a North African boy (A). Dermoscopy displays polygonal, flat, brown globules separated by whitish/pale striae creating a “cobblestone pattern” (“crocodile skin-like” appearance) (magnification in the inset) (B). (Courtesy of Enzo Errichetti, MD – Udine, Italy.)

A

B

FIGURE 5.29  Gougerot-Carteaud syndrome in an Indian man (A). Dermoscopic examination reveals sulci and gyri giving rise to a “cerebriform pattern” (magnification in the inset) (B). (Courtesy of Balachandra Ankad, MD – Bagalkot, India.)

72

Hyperpigmented dermatoses joints, especially shoulders and elbows, are the main involved sites.36

5.17  Nevus of Ota and Becker nevus 5.17.1 Introduction Nevus of Ota is a dermal melanocytosis distributed along the trigeminal nerve’s ophthalmic and maxillary branches, whereas Becker nevus is a cutaneous hamartoma usually presenting in late childhood or early adolescence and persisting through life once it is fully evolved.36 A role of androgens with increased expression of androgen receptors has been hypothesized in the pathogenesis of the latter condition.36

5.17.2  Clinical presentation Nevus of Ota (Figure  5.30A) usually presents as unilateral, mottled, bluish-grey or bluish-brown macules over the zygomatic and temporal areas since birth, although it can present as bilateral macules or onset in adolescence.36 Additionally, the oral mucosa and sclera can be involved. On the other hand, Becker nevus (Figures  5.31A and 5.32B) manifests as a circumscribed hyperpigmented patch with a variable degree of hypertrichosis on and around the lesion; areas near the large A

5.17.3 Dermoscopy Dermoscopy of nevus of Ota (Figure 5.30B) typically reveals a patchy distribution of brown to grey structureless areas with ostial sparing (pseudonetwork), histologically corresponding to pigmented dendritic melanocytes and melanophages that dissect the bundles of dermal collagen in the dermis (more superficial for brown areas and deeper for grey areas).6,37 Importantly, such dermoscopic features may also be seen in melasma, but in nevus of Ota the shade of the pigmented structures is more variegated and may be associated with ostial obliteration.6,37 Interostial pigmented dots and perifollicular hypopigmentation may also be found less commonly.6,37 The dermoscopic features of Becker nevus (Figures  5.31B and 5.32B) include a brown network or blotchy areas, terminal hairs and perifollicular hypopigmentation.38,39 Additionally, skin furrow hypopigmentation and white structureless areas (Figure  5.32B) may also be observed. Pigmentary structures in Becker nevus correspond to basal layer pigmentation.38,39

B

FIGURE 5.30  Nevus of Ota in an Indian woman (A). Dermoscopy: multifocal brown and grey pigmentation with ostial sparing (pseudonetwork) (B).

A

B

FIGURE 5.31  Becker nevus in an Indian boy (A). Dermoscopic assessment shows brown reticular areas with perifollicular hypopigmented areas and terminal hairs (B).

73

Dermoscopy for skin of colour A

B

FIGURE 5.32  Becker nevus in a North African boy (A). Dermoscopy displays blotchy brown structureless areas with perifollicular hypopigmented areas, white structureless areas and terminal hairs (B). (Courtesy of Enzo Errichetti, MD – Udine, Italy.)

Acknowledgment Special thanks go to Balachandra Ankad for writing the Sections 5.5 (Friction melanosis) and 5.16 (Gougerot-Carteaud syndrome).

REFERENCES 1. Robles‐Méndez JC, Rizo‐Frías P, Herz‐Ruelas ME, Pandya AG, Ocampo Candiani J. Lichen planus pigmentosus and its variants: Review and update. Int J Dermatol 2018;57:505–14. 2. Mathews I, Thappa DM, Singh N, Gochhait D. Lichen planus  pigmentosus: A  short review. Pigment Int ­ 2016;3:5–10. 3. Neema S, Jha A. Lichen planus pigmentosus. Pigment Int 2017;4:48–9. 4. Rodrigues M, Pandya AG, Bekkenk M, Parsad D, Kumarasinghe SP. Current understanding of lichen planus pigmentosus, erythema dyschromicum perstans (ashy dermatosis), and idiopathic eruptive macular pigmentation. Pigment Int 2019;6:4–8. 5. Chatterjee M, Neema S. Dermoscopy of pigmentary disorders in brown skin. Dermatol clin 2018;36:473–85. 6. Errichetti E, Ankad BS, Sonthalia S, et  al. Dermoscopy in general dermatology (non-neoplastic dermatoses) in skin of colour: A  comparative retrospective study by the International Dermoscopy Society. Eur J Dermatol 2020. doi: 10.1684/ejd.2020.3928 7. Errichetti E, Angione V, Stinco G. Dermoscopy in assisting the recognition of ashy dermatosis. JAAD Case Reports 2017;3:482–4. 8. Gupta V, Sharma VK. Ashy dermatosis, lichen planus pigmentosus and pigmented cosmetic dermatitis: Are we splitting the hair? Indian J Dermatol Venereol Leprol 2018;84:470–4. 9. Mahajan SH, Mahajan SA, Khopkar US, Kharkar VD. Follicular dowling – Degos disease: A rare pigmentary dermatosis. Indian Dermatol Online J 2017;8:487–9.

10. Zhang J, Li M, Yao Z. Updated review of genetic reticulate pigmentary disorders. Br J Dermatol 2017;177:945–59. 11. Nirmal B, Dongre AM, Khopkar US. Dermatoscopic features of hyper and hypopigmented lesions of Dowling Degos disease. Indian J Dermatol 2016;61:125. 12. Geißler S, Dyall‐Smith D, Coras B, Guther S, Peters B, Stolz W. Unique brown star shape on dermatoscopy of generalized Dowling‐Degos disease. Australas J Dermatol 2011;52:151–3. 13. Errichetti E, Lallas A. Other infiltrative conditions. In: Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press, 2018:173–7. 14. Kaliyadan F, Alkhateeb A, Kuruvilla J, Swaroop K, Alabdulsalam AA. Dermoscopy of primary cutaneous amyloidosis in skin of colour. Dermatol Pract Concept 2019;9:232–34. 15. Mutalik SD, Pethe S V, Nikam BP, Rasal YD. Facial frictional melanosis in Indian patients: Defining the entity. Clin Dermatol Rev 2019;3:78–83. 16. Errichetti E, Stinco G. Dermoscopy in general dermatology: A  practical overview. Dermatol Ther (Heidelb) 2016;6:471–507. 17. Stiube A, Jenni D, Wiederkehr L, Anzengruber F, Nobbe S. Terra Firme-Forme dermatosis diagnostic sign and treatment: A case report. Case Rep Dermatol 2019;11:108–12. 18. Errichetti E, Stinco G. Dermoscopy in terra firma-forme dermatosis and dermatosis neglecta. Int J Dermatol 2017;56:1481–83. 19. Kang HY, Bahadoran P, Suzuki I, et  al. In vivo reflectance confocal microscopy detects pigmentary changes in melasma at a cellular level resolution. Exp Dermatol 2010;19:e228–e33. 20. Gupta T, Sarkar R. Dermoscopy in melasma-is it useful? Pigment Int 2017;4:63–4. 21. Sonthalia S, Jha AK, Langar S. Dermoscopy of melasma. Indian Dermatol Online J 2017;8:525–6. 22. Errichetti E. Dermoscopy in Monitoring and predicting therapeutic response in general dermatology (non-tumoral

74 dermatoses): An up-to-date overview. Dermatol Ther (Heidelb) 2020;10:1199–214. 23. Sindhu CS, Babitha C, Priyadarshini A, Veeraraghavan M. Exogenous ochronosis in an elderly Indian male: A  case report. Pigment Int 2019;6:33–6. 24. Khunger N, Kandhari R. Dermoscopic criteria for differentiating exogenous ochronosis from melasma. Indian J Dermatol Venereol Leprol 2013;79:819–21. 25. Shenoi SD, Rao R. Pigmented contact dermatitis. Indian J Dermatol Venereol Leprol 2007;73:285–7. 26. Turan E, Cimen V, Kutlu Haytoglu NS, Göde ED, Gürel MS. A case of bullous erythema ab Igne accompanied by anemia and subclinical hypothyroidism. Dermatol Online J 2014;20:22336. 27. Russo F, Flori ML, Taddeucci P, Rubegni P, Cinotti E. Pigmentary demarcation lines of Voigt-Futcher: Dermoscopic and reflectance confocal microscopy features. Skin Res Technol 2020;26:440–2. 28. Phiske MM. An approach to acanthosis nigricans. Indian Dermatol Online J 2014;5:239–49. 29. Savory SA, Pandya AG. Post-inflammatory hyperpigmentation. In: Dermatology Atlas for Skin of Colour (Jackson-Richards D, Pandya AG, eds), 1st edn. Berlin: Springer-Verlag, 2014:21–6. 30. Verma SB, Vasani RJ, Chandrashekar L, Thomas M. Seborrheic melanosis: An entity worthy of mention in dermatological literature. Indian J Dermatol Venereol Leprol 2017;83:285–9.

Hyperpigmented dermatoses 31. Arshdeep, Sonthalia S, Kaliyadan F, Errichetti E, Jha AK, Lallas A. Seborrheic melanosis and dermoscopy: Lumping better than splitting. Indian J Dermatol Venereol Leprol 2018;84:585–7. 32. Lim JH, Tey HL, Chong WS. Confluent and reticulated papillomatosis: Diagnostic and treatment challenges. Clin Cosmet Investig Dermatol 2016;9:217–23. 33. Jackson-Richards D. Confluent and reticulated papillomatosis. In: Dermatology Atlas for Skin of Colour (Jackson-Richards D, Pandya AG, eds), 1st edn. Berlin: Springer-Verlag, 2014:45–8. 34. Ankad BS, Dombale V, Sujana L. Dermoscopic patterns in confluent and reticulated papillomatosis: A case report. Our Dermatol Online 2016;7:323–6. 35. Errichetti E, Maione V, Stinco G. Dermatoscopy of confluent and reticulated papillomatosis (Gougerot-Carteaud syndrome). J Dtsch Dermatol Ges 2017;15:836–8. 36. Kromann AB, Ousager LB, Ali IKM, Aydemir N, Bygum A. Pigmentary mosaicism: A review of original literature and recommendations for future handling. Orphanet J Rare Dis 2018;13:39. 37. Elmas ÖF, Kilitçi A. Dermoscopic findings of nevus of Ota. Balkan Med J 2020;37:116–18. 38. Nair PA, Modasia K, Bhavsar N, Navadiya R. Dermatoscopy of Becker’s nevus. Egypt J Dermatol Venerol 2019;39:37–9. 39. Ingordo V, Iannazzone SS, Cusano F, Naldi L. Dermoscopic features of congenital melanocytic nevus and Becker nevus in an adult male population: An analysis with a 10-fold magnification. Dermatology 2006;212:354–60.

6 Hypopigmented dermatoses

Hypopigmented dermatoses

Dermoscopy for skin of colour

Shekhar Neema

6.1 Vitiligo 6.1.1 Introduction Vitiligo is an acquired depigmentary disorder causing a progressive reduction in melanocyte number that shows an incidence rate of 0.5% to 2% worldwide, although it may reach 8.8% in Indians.1,2 Its etiopathogenesis is still unclear, albeit cytotoxic/biochemical, neural and autoimmune factors would be involved.1,2

6.1.2  Clinical presentation Vitiligo (Figures  6.1A–6.3A and 6.5A) is clinically characterized by milk-white macules/patches with convex borders mainly involving the face, neck, forearms, feet, dorsal hand, fingers and sites of trauma (Koebner phenomenon); hair in vitiliginous areas may be white.1,2 Two main clinical subtypes are recognized, namely segmental and non-segmental forms.1,2 Less frequent variants include trichrome, quadrichrome, pentachrome, blue and inflammatory vitiligo.1,2 Vitiligo can be clinically classified as unstable (development of new lesions, progression of existing lesions and presence of Koebner phenomenon) or stable (absence of the aforementioned findings for more than one year).1,2 Additionally, vitiligo lesions can also be classified as evolving or fully evolved, though both of them can be present in each patient.1,2

6.1.3 Dermoscopy Milky/bright white structureless areas with sharp and convex margins are the main dermoscopic findings in vitiligous A

lesions, yet dermoscopic features of vitiligo in dark-skinned patients classically vary according to the disease stage.3–6 In detail, evolving/early lesions (Figure 6.1B) are characterized by a reduced pigmentary network, reversed pigmentary network, perilesional hyperpigmentation and perifollicular pigment (although the last two findings may also be seen in repigmenting phases), whereas fully evolved patches (Figure 6.2B) typically show an absent pigmentary network, diffuse white milky/bright background and leukotrichia (white hair).3–6 Additionally, dermoscopic examination may also help assessment of disease stability as stable lesions are mainly characterized by a sharp border, but also have perilesional and/ or perifollicular hyperpigmentation (Figures  6.3B), whereas unstable lesions typically display irregular and/or less defined borders giving rise to specific patterns (i.e., trichrome, “starburst” and “comet tail”) (Figure 6.4A), the presence of small white globules in perilesional skin (described as satellites, confetti-like pattern and “tapioca sago” appearance) (Figure 6.4B) and micro-Koebner phenomenon (i.e., the occurrence of isomorphic depigmented streaks along the line of trauma around the main vitiligo patch) (Figure 6.5B).3–7 Besides diagnostic purposes, dermoscopy may assist in choosing the therapy (e.g., surgical treatments are usually used in stable disease), predicting clinical response to treatments (e.g., white hair and perifollicular pigmentation are respectively related to poor and good outcomes) and monitoring therapeutic results (as it may reveal increases in perilesional and intralesional pigmentation before they become evident on clinical grounds).7

B

FIGURE 6.1  Vitiligo (evolving/early lesions) in an Indian patient (A). Dermoscopy: milky white area with ill-defined margins (B).

DOI: 10.1201/9780367816483-6

76 A

Hypopigmented dermatoses B

FIGURE 6.2  Vitiligo (fully evolved patches) of the leg in an Indian boy (A). Dermoscopy: absent pigmentary network, well-defined white milky/ bright background and leukotrichia (white hair) (B).

A

B

FIGURE 6.3  Vitiligo of the forearm (stable lesions) in an Indian man (A). Dermoscopy: sharp milky white background with a reduced pigmentary network and perifollicular pigmentation (B).

A

B

FIGURE 6.4  Dermoscopy of unstable vitiliginous lesions. Bright white areas with irregular (“starburst” pattern) and ill-defined borders; two different shades of white are seen giving rise to a “trichrome” pattern (A). Reduced pigmentary network over an ill-defined white background along with the presence of small white globules in perilesional skin (B).

77

Dermoscopy for skin of colour A

B

FIGURE 6.5  Vitiligo of the back in an Indian girl (A). Dermoscopy shows the “micro-Koebner” phenomenon (i.e., occurrence of isomorphic depigmented streaks along the line of trauma around the main vitiligo patch) (B).

6.2  Idiopathic guttate hypomelanosis 6.2.1 Introduction Idiopathic guttate hypomelanosis (IGH) is a benign, asymptomatic hypopigmented dermatosis in which chronic exposure to ultraviolet rays and senile degeneration would play a relevant pathogenetic role.8

6.2.2  Clinical presentation IGH is characterized by multiple, discrete round or oval, 2–5  mm in diameter, porcelain-white macules mainly distributed over the sun-exposed areas of the extremities (Figure 6.6A) and, less commonly, on the trunk; involvement of sun-covered areas is also possible. Such a condition generally affects older populations.8 Three morphological variants of IGH have been described, including: (I) hypopigmented macules on a background of sundamaged skin in sun-exposed areas; (II) ivory white, discrete, stellate, sclerotic macules with distinct margins, both over sun-exposed and covered/sun-protected areas; and (III) small hypopigmented macules with distinct margins and hyperkeratotic flat crust, usually with a scalloped border.8

6.2.3 Dermoscopy From a dermoscopic point of view, IGH in skin of colour is characterizing by bright white areas with sharp margins along with brown circles around eccrine glands openings and peripheral white projections (configuring several morphologies, metaphorically described as “ameboid”, “petaloid” and “feathery” pattern) (Figures  6.6B and 6.7A), with the last two features being characteristic of such a diagnosis.6,9,10 Notably, the presence of perieccrine pigmentation would be because of a higher resistance of peri-eccrine melanocytes to sun-induced damage.6,9,10 In recent lesions, ill-defined

white areas (known as “nebuloid” pattern) may also be seen (Figure 6.7B).6,9,10 Additional poorly specific dermoscopic findings include perifollicular pigmentation and an intralesional brown network.6,9,10 Interestingly, unlike in fair skin, IGH in darker phototypes do not feature a perilesional brown network, likely because they are less prone to sun-induced hyperpigmentation.6,9,10

6.3  Progressive macular hypomelanosis 6.3.1 Introduction Progressive macular hypomelanosis (PMH) is an acquired disorder causing hypopigmentation thought to be related to Propionibacterium acnes growth in the pilosebaceous unit.11 It is more commonly seen in adolescents and young adults with dark skin.11

6.3.2  Clinical presentation It typically manifests as asymptomatic hypopigmented illdefined macules mainly localized over the trunk (Figure 6.8A), without any previous history of inflammation or injury.11 The natural course of the disease is not clear, with lesions disappearing spontaneously within 3–5 years in a fourth of cases.11

6.3.3 Dermoscopy Dermoscopy of PMH reveals a non-scaly, smooth, ill-defined whitish area (Figure  6.8B) histologically corresponding to a reduction in melanin in the affected skin with a normal melanocyte number.6,12 Such a pattern may help distinguish this condition from its main clinical differential diagnosis, i.e., achromic pityriasis versicolour (mainly characterized by white scales in the skin furrows or around the hair over a white background).6,12 A  reverse pigmentary network and perifollicular white areas may also be observed (Figure 6.8B).

78

Hypopigmented dermatoses A

B

FIGURE 6.6  Idiopathic guttate hypomelanosis of the forearm in an Indian woman (A). Dermoscopic examination reveals well-defined white areas displaying peripheral projections (arrows) and periostial pigmentation (brown circles) (arrowheads) inside (B).

A

B

FIGURE 6.7  Dermoscopy of idiopathic guttate hypomelanosis. Well-defined white areas with peripheral projections (arrows) in an established lesion (A). Ill-defined white areas (known as “nebuloid” pattern) is visible in a recent lesion (B).

A

B

FIGURE 6.8  Clinical image of progressive macular hypomelanosis (A). Dermoscopic examination reveals non-scaly, smooth, discrete to confluent, ill-defined white areas; a reverse pigmentary network and perifollicular white areas are also evident (B).

79

Dermoscopy for skin of colour

6.4  Postinflammatory hypopigmentation 6.4.1 Introduction Postinflammatory hypopigmentation (PIH) is an acquired loss of pigmentation of the skin that is particularly common in dark phototypes.13 It may be secondary to cutaneous inflammatory disorders, irritations, burns, freezing or dermatological procedures.13

6.4.2  Clinical presentation PIH is typified by ill-defined defined white macules/patches with an irregular outline (Figures  6.9A–6.11A), yet it differs according to the original dermatosis.13 The degree of whitening may vary from partial to total loss of pigment, whereas the surface may be smooth or scaly.13 A

6.4.3 Dermoscopy Besides an ill-defined white background (histologically corresponding to a decrease in epidermal melanin) (Figures 6.9B–6.11B), dermoscopy of PIH may show features typical of the original lesions, thereby assisting the retrospective diagnosis.12 In particular, PIH secondary to psoriasis and prurigo nodularis may respectively display uniform dotted vessels or star-like depigmentation.12 When it comes to discoid erythematous lupus, postinflammatory hypopigmented lesions typically feature bright white areas (histologically corresponding to dermal fibrosis) as well as hyperpigmentation (e.g., radial brown streaks, brown structureless areas, perifollicular pigmentation or a honeycomb brown network) (Figure 6.11B); linear branching vessels to dotted/polymorphous vessels may also be seen.12

B

FIGURE 6.9  Postinflammatory hypopigmentation after treatment of atopic dermatitis in an Indian man (A). Dermoscopy: ill-defined white areas alternating with normal pigment network (B).

A

B

FIGURE 6.10  Clinical image shows depigmentation resulting from a scald injury (post-burn depigmentation) (A). Dermoscopy shows a well-defined area of hypopigmentation; the absence of hair and follicular and eccrine openings are indicators that depigmentation is due to scarring (B).

80 A

Hypopigmented dermatoses B

FIGURE 6.11  Clinical image of discoid lupus erythematosus (DLE) (scarring hypopigmented lesions) (A). Dermoscopic assessment displays a bright white background along with brown dots, focal structureless areas and follicular plugs, with the latter being characteristic of active DLE lesions (B).

6.5  Achromic nevus and hypomelanosis of Ito 6.5.1 Introduction Achromic nevus (AN), also known as nevus depigmentosus, and hypomelanosis of Ito (HI) are two forms of cutaneous mosaicism resulting in localized hypopigmented skin lesions, with the latter possibly associated with extracutaneous involvement.14 They are usually present at birth, yet they may sometimes become evident during childhood.14

sharpness of the margins may vary in the context of the lesion, unlike vitiligo.6,14 Importantly, the most characterizing feature of both such conditions is represented by the presence of an intralesional brown network (“islands of spared skin”) (Figures 6.12B and 6.13B).6,14 Additional findings include peripheral white projections (“pseudopods”) and pigmentation around the eccrine ostia.6,14

6.6  Ash-leaf macules 6.5.2  Clinical presentation

6.6.1 Introduction

AN typically presents as an asymptomatic white patch of variable size having well-defined irregular margins; satellite white macules are often present around the main lesion giving rise to a “splash of paint”-like appearance (Figure 6.12A).14 Variants include segmental, linear and systematized AN.14 HI is characterized by asymmetrical streaky, patchy, whorl-like, or linear white patches in a “marble cake pattern” along the lines of Blaschko, commonly involving the trunk (Figure 6.13A), though the extremities or face may be affected more rarely.14

Ash leaf macules (ALMs) are hypopigmented lesions that may be seen in healthy people, yet the presence of ≥3 ALMs of at least 5  mm in size is one of the major diagnostic criteria of tuberous sclerosis.15

6.5.3 Dermoscopy Dermoscopy of AN and HI reveals similar findings, with a bright white (Figure  6.12B) or dull white (more commonly) (Figure  6.13B) area having sharp- (more commonly) or illdefined, irregular (serrated) borders being the most common pattern.6,14 Notably, the shade of the white background and the

6.6.2  Clinical presentation The name of ALMs comes from their resemblance to the leaf of the eastern mountain ash tree, as they are shaped as a long oval with one rounded and one tapered end (Figure 6.14A).15

6.6.2 Dermoscopy Dermoscopic features differentiate ALM from achromic nevus and are characterized by a faint reticular network within areas of total loss of pigment pattern (Figure 6.14B) (author’s personal observations).

81

Dermoscopy for skin of colour A

B

FIGURE 6.12  Clinical image of achromic nevus involving the middle finger in an Indian boy (A). Dermoscopy: bright white background having sharp-defined, irregular (serrated) borders and intralesional brown network (“islands of spared skin”) and pigmentation around the eccrine ostia (arrows) (B).

A

B

FIGURE 6.13  Hypomelanosis of Ito in an Indian boy (A). Dermoscopy: dull white background having ill-defined, irregular (serrated) borders and intralesional brown network (“islands of spared skin”).

A

B

FIGURE 6.14  Ash leaf macule in an Indian boy (A). Dermoscopy: faint reticular network within areas of total loss of pigment pattern (B).

82 A

Hypopigmented dermatoses B

FIGURE 6.15  Hypopigmented lepromatous lesion of the forearm in an Indian man (A). Dermoscopic examination reveals a dull white background having ill-defined margins and intralesional eccrine pigmentation (“spared” areas); reduction of the appendages (visible as a lack of hairs and sweat gland ostia) is also seen (B).

6.7  Hypopigmented leprosy

consistent with the perifollicular trophism of granulomatous infiltrate.16

6.7.1 Introduction Leprosy is a chronic granulomatous disease affecting the skin and nerves caused by Mycobacterium leprae.16 It may present with hypopigmented patches, especially borderline tuberculoid and indeterminate leprosy.16

6.8  Pityriasis alba 6.8.1 Introduction Pityriasis alba is an acquired hypopigmented disorder commonly observed in atopic patients during childhood.17

6.7.2  Clinical presentation Hypopigmented lepromatous lesions typically manifest as one or multiple ill-defined hypopigmented macules or patches (Figure  6.15A) characterized by anaesthesia or hypoaesthesia.16 Not uncommonly, they are mistaken for other common hypopigmented dermatoses.16

6.8.2  Clinical presentation

6.7.3 Dermoscopy

6.8.3 Dermoscopy

Dermoscopy of hypopigmented leprosy usually shows a dull white background having ill-defined margins; intralesional brown reticular areas and perifollicular/perieccrine pigmentation (“spared” areas) may also be seen (Figure  6.15B).16 However, the hallmark of hypopigmented lepromatous lesions is the reduction of the appendages (visible as a lack of hairs and sweat gland ostia) in the absence of fibrosis/ulceration (Figure  6.15B).16 This is related to the peculiar tendency of the disease to destroy the skin appendages.16 Finally, during the initial stages, the perifollicular hypopigmentation may be the only dermoscopic finding of hypopigmented leprosy,

The main dermoscopic feature of pityriasis alba is represented by ill-defined dull white areas (Figures  6.16B and 6.17B).6 Such a finding is often associated with white scales (patchy or diffuse in skin furrows) and incomplete residual pigmentation (semicircles) around eccrine ostia (Figures  6.16B and 6.17B), with the latter finding being found to be characteristic of facial pityriasis alba diagnosis when compared with other similar hypopigmented dermatoses.6 This association would be related to a partial resistance to exfoliation of the melanin located around the eccrine sweat glands. Brown dots are also sometimes seen.6

It manifests as asymptomatic, ill-defined, hypopigmented macules/patches, often having a scaly surface, that usually involve the face (Figure  6.16A), thighs and, less commonly, the trunk (Figure 6.17A).17

83

Dermoscopy for skin of colour A

B

FIGURE 6.16  Pityriasis alba involving the face of an African man (A). Dermoscopy shows ill-defined dull white areas along with incomplete residual pigmentation (semicircles) around eccrine ostia inside the lesion (arrows) (B). (Courtesy of Enzo Errichetti, MD – Udine, Italy.)

A

B

FIGURE 6.17  Pityriasis alba of the trunk in an African girl (A). Ill-defined dull white areas along with intralesional incomplete residual pigmentation (semicircles) around eccrine ostia (arrow) (B). (Courtesy of Enzo Errichetti, MD – Udine, Italy.)

REFERENCES 1. Vora R V, Patel BB, Chaudhary AH, Mehta MJ, Pilani AP. A clinical study of vitiligo in a rural set up of Gujarat. Indian J community Med 2014;39:143–6. 2. Sehgal VN, Srivastava G. Vitiligo: Compendium of clinico-epidemiological features. Indian J Dermatol Venereol Leprol 2007;73:149–56. 3. Thatte SS, Khopkar US. The utility of dermoscopy in the diagnosis of evolving lesions of vitiligo. Indian J Dermatol Venereol Leprol 2014;80:505–8. 4. Chatterjee M, Neema S. Dermoscopy of pigmentary disorders in brown skin. Dermatol Clin 2018;36:473–85. 5. Nirmal B, Antonisamy B, Peter CVD, George L, George AA, Dinesh GM. Cross-sectional study of dermatoscopic

findings in relation to activity in vitiligo: BPLeFoSK criteria for stability. J Cutan Aesthet Surg 2019;12:36–41. 6. Errichetti E, Ankad BS, Sonthalia S, et  al. Dermoscopy in general dermatology (non-neoplastic dermatoses) in skin of colour: A comparative retrospective study by the International Dermoscopy Society. Eur J Dermatol 2020. doi: 10.1684/ ejd.2020.3928 7. Errichetti E. Dermoscopy in monitoring and predicting therapeutic response in general dermatology (non-tumoral dermatoses): An up-to-date overview. Dermatol Ther (Heidelb) 2020;10:1199–214. 8. Kumarasinghe P. Idiopathic guttate hypomelanosis. In: Dermatological cryosurgery and cryotherapy (Abramovits W, Graham G, Har-Shai Y, Strumia R, eds), 1st edn. London: Springer, 2016:407–11.

84 9. Ankad BS, Beergouder SL. Dermoscopic evaluation of idiopathic guttate hypomelanosis: A  preliminary observation. Indian Dermatol Online J 2015;6:164–7. 10. Errichetti E, Stinco G. Dermoscopy of idiopathic guttate hypomelanosis. J Dermatol 2015;42:1118–9. 11. Thng STG, Long VSH, Chuah SY, Tan VWD. Efficacy and relapse rates of different treatment modalities for progressive macular hypomelanosis. Indian J Dermatol Venereol Leprol 2016;82:673–6. 12. Errichetti E, Stinco G. Dermoscopy in general dermatology: A  practical overview. Dermatol Ther (Heidelb) 2016;6:471–507.

Hypopigmented dermatoses 13. Vachiramon V, Thadanipon K. Postinflammatory hypopigmentation. Clin Exp Dermatol 2011;36:708–14. 14. Ankad B, Shah S. Dermoscopy of nevus depigmentosus. Pigment Int 2017;4:121–3. 15. Cardis MA, DeKlotz CMC. Cutaneous manifestations of tuberous sclerosis complex and the paediatrician’s role. Arch Dis Child 2017;102:858–63. 16. Ankad BS, Sakhare PS. Dermoscopy of borderline tuberculoid leprosy. Int J Dermatol 2018;57:74–6. 17. Baselga E. Disorders of hypopigmentation. In: Pediatric Dermatology (Schachner LA, Hansen RC, eds), 4th edn. Philadelphia: Elsevier, 2011:724.

7 Primary cutaneous lymphomas

Primary cutaneous lymphomas

Dermoscopy for skin of colour

Tomas Huerta and Trilokraj Tejasvi

7.1  Mycosis fungoides

7.1.3 Dermoscopy

7.1.1 Introduction

MF in skin of colour is usually characterized by striking pigmentary changes. In detail, dark-brown to black thick lines forming pseudonetworks, dots, globules and structureless areas interrupted by prominent eccrine duct openings are typically visible in both patches and plaques (Figures 7.1B–7.3B) (authors’ personal observations). From a histological point of view, pigmented structures would be related to basal layer hyperpigmentation and dermal pigment incontinence.3–9 Additionally, geometric white lines (histologically related to acanthosis/dermal fibrosis) (Figures  7.2B–7.4B), patchy pink-red areas (resulting from vessels dilation) (Figure 7.4B), as well as white rosettes (Figures 7.2B and 7.4B) and follicular plugs surrounded by hyperpigmented to violaceous halos (Figure  7.4B) may also be seen in the plaque-stage/tumoral stage (authors’ personal observations). Of note, the last two findings may be indicative of folliculotropism, but are also observed in classic MF as a result of follicular hyperkeratosis (Figure 7.5).10–12 Large, yellow-grey amorphous structures with ridges may be seen in verrucous MF (Figure  7.3B), whereas hypopigmented MF may show ill-defined white-pink areas (with complete loss of the natural pigment network), whose shade is often variable in the context of the same hypopigmented patch (Figure  7.6B) (authors’ personal observations). Finally, in erythrodermic cutaneous T-cell lymphomas (CTCLs) and Sezary syndrome, the presence of serpiginous vessels has been reported to help differentiate such entities from other common causes of erythroderma in Caucasians.13 However, in skin of colour, the vessels’ morphology is difficult to discern, and diagnosis is predominantly based on pigmentary alterations as described previously; hypopigmented areas with reduction/ absence of the physiological brown network and haemorrhagic dots/globules may also be seen (Figure  7.7B) (authors’ personal observations).

Mycosis fungoides (MF) is the most common cutaneous T-cell lymphoma, whose incidence has been reported to be higher in African Americans compared with light phototypes.1–3 Additionally, in the former ethnicity, it is often associated with earlier onset and increased mortality.1–3 The aetiology of MF is still not completely known, with persistent antigenic factors and viral agents being considered as possible causes for malignant transformation of T cells.1–3

7.1.2  Clinical presentation MF classically presents with erythematous, scaly patches (patch stage) (Figure  7.1A) that progress to plaques (plaque stage) (Figures  7.2A and 7.3A) and tumours (tumoral stage) (Figure 7.4A) over several years. Erythrodermic variants may also be seen (Figure 7.7A).3–9 In skin of colour, classic features include arcuate, annular patches/plaques >5 cm associated with polymorphic pigmentation (Figures  7.1A–7.3A).3–9 With progressive infiltration, plaques exhibit a variety of secondary changes and may develop a lichenified, leathery or verrucous appearance.3–9 Hypopigmented MF (Figure  7.6A) is not infrequent in dark-skinned patients, especially younger patients of African, Arab and South-East Asian descent, and commonly presents as strikingly diffuse hypopigmented patches on sun-exposed sites.3–9 On the other hand, folliculotropic MF manifests as follicular-based papules, acneiform papules and pustules, alopecic patches and/or hyperpigmented plaques. Additional morphologic variants include hyperpigmented and pigmented purpuric MF.6–8 Clinical features such as “leonine” facies and painful palm and sole involvement can occur in advanced stage MF and Sezary syndrome.3

DOI: 10.1201/9780367816483-7

86

Primary cutaneous lymphomas A

B

FIGURE 7.1  Patch-stage mycosis fungoides in an African American man (A). Dermoscopic examination reveals dark-brown, thick lines forming a pseudonetwork (brown structureless areas interrupted by prominent eccrine duct openings) (B).

A

B

FIGURE 7.2  Plaque-stage mycosis fungoides in an African American woman (A). Dermoscopy shows dark-brown to black thick lines forming pseudonetworks and dots along with geometric white lines and white rosettes (B).

A

B

FIGURE 7.3  Plaque-stage mycosis fungoides with verrucous aspect in an African American woman (A). Dermoscopy: dark-brown lines forming pseudonetworks and bright white lines are seen at the periphery of the plaque; yellow-grey amorphous keratotic mass (B).

87

Dermoscopy for skin of colour A

B

FIGURE 7.4.  Tumoral/plaque-stage mycosis fungoides in an African American woman (A). Dermoscopy: geometric white lines surrounding follicular white rosettes plugs surrounded by violaceous halos (B).

A

B

FIGURE 7.5  Follicular plugs on dermoscopy indicative of follicular hyperkeratosis in classic mycosis fungoides (A) or folliculotropic mycosis fungoides (B).

A

B

FIGURE 7.6  Hypopigmented mycosis fungoides in an African American boy (A). Dermoscopy reveals ill-defined white-pink areas (with complete loss of the natural pigment network), whose shade is variable in the context of the patch (B).

88

Primary cutaneous lymphomas A

B

FIGURE 7.7.  Erythrodermic mycosis fungoides in an Indian man (A). Dermoscopic assessment displays brown lines (arrows), hypopigmented patches devoid of brown network and haemorrhagic dots/globules (B). (Courtesy of Enzo Errichetti, MD – Udine, Italy.)

7.2  Other cutaneous lymphomas 7.2.1 Introduction Non-MF skin lymphomas include both CTCLs and cutaneous B-cell lymphomas (CBCLs).3,4,9 In contrast to MF, no significant differences between dark- and fair-skinned subjects are reported when it comes to the incidence of such lymphomas.3,4,9 Their pathogenesis is mostly unknown, yet it is postulated that an accumulation of genetic alterations leads to clonal proliferation and malignant transformation of skin-homing T cells in CTCLs, whereas chronic antigenic stimulation and immune dysregulation have been speculated to play a role in CBCLs.3,4,9

7.2.2  Clinical presentation Non-MF CTCLs exhibit a wide variety of clinical presentations, with primary cutaneous CD30+ lymphoproliferative disorders (the most common subtypes) presenting with solitary/multiple, brownish/purple, ulcerative nodules (primary cutaneous anaplastic large cell lymphoma) or self-resolving/ recurrent crops of brownish/purple papules/nodules evolving into hyperpigmented scars (lymphomatoid papulosis) (Figure 7.8A).3,4 CBCLs are most commonly present with violaceous, solitary or grouped papules or nodules on the head and neck area.3,4,9 Although the incidence of CBCL is extremely low in African Americans, these patients tend to present with regional or generalized cutaneous involvement, although the rates of

extracutaneous systemic disease have been comparable to that of whites in small case series.3,4,9

7.2.3 Dermoscopy Little data is available on dermoscopy of non-MF CTCL and CBCL occurring in dark phototypes. According to a study investigating solitary nodular/tumoral CTCL and CBCL in Chilean and Brazilian patients, orange colour (due to the compact cells infiltrate), follicular plugs (corresponding to follicular hyperkeratosis) and multiple vessel morphologies (resulting from dermal vessels dilation) are the most commonly encountered dermoscopic features, with the first two findings being more specific when comparing such lymphomas with controls (especially non-pigmented basal cell carcinoma and amelanotic melanoma).14–16 Notably, in very dark skin types, the vessels are difficult to appreciate as the high melanin content prevents the light of the dermatoscope from penetrating beyond the basal layer of the epidermis (authors’ personal observation). When it comes to lymphomatoid papulosis, dermoscopic patterns typically vary according to the disease stage.17 Early lesions generally feature dotted or tortuous/irregular vessels (corresponding to dermal vessels dilation), whereas a central yellow or brown crust, respectively resulting from hyperkeratosis or necrosis, and a peripheral white collarette scaling are seen in mature lesions.17 Additionally, a central erosion displaying vessels of mixed morphologies may also be visible in well-developed papules (Figure 7.8B).17 Finally, brown-grey structureless areas are often seen as the result of postinflammatory pigmentation.17

89

Dermoscopy for skin of colour A

B

FIGURE 7.8  Lymphomatoid papulosis in an Indian woman (A). Dermoscopic examination shows a central erosion displaying vessels of mixed morphologies and peripheral white scaling collarette in a well-developed papule (B). (Courtesy of Enzo Errichetti, MD – Udine, Italy.)

REFERENCES















1. Su C, Nguyen KA, Bai HX, et al. Racial disparity in mycosis fungoides: An analysis of 4495 cases from the US national cancer database. J Am Acad Dermatol 2017;77:497–502. 2. Wilson LD, Hinds GA, Yu JB. Age, race, sex, stage, and incidence of cutaneous lymphoma. Clin Lymphoma Myeloma Leuk 2012;12:291–6. 3. Hinds GA, Heald P. Cutaneous T-cell lymphoma in skin of colour. J Am Acad Dermatol 2009;60:359–75. 4. Rubio-Gonzalez B, Zain J, Rosen ST, et al. Clinical manifestations and pathogenesis of cutaneous lymphomas: Current status and future directions. Br J Haematol 2017;176:16–36. 5. Lambroza E, Cohen SR, Phelps R, Lebwohl M, Braverman IM, DiCostanzo D. Hypopigmented variant of mycosis fungoides: Demography, histopathology, and treatment of seven cases. J Am Acad Dermatol 1995;32:987–93. 6. Pavlovsky L, Mimouni D, Amitay-Laish I, et  al. Hyperpigmented mycosis fungoides: An unusual variant of cutaneous T-cell lymphoma with a frequent CD8+ phenotype. J Am Acad Dermatol 2012;67:69–75. 7. Price NM, Fuks ZY, Hoffman TE. Hyperkeratotic and verrucous features of mycosis fungoides. Arch Dermatol 1977;113:57–60. 8. Barnhill RL, Braverman IM. Progression of pigmented purpura-like eruptions to mycosis fungoides: Report of three cases. J Am Acad Dermatol 1988;19:25–31. 9. Geller S, Pulitzer M, Myskowski P, Kheterpal MJ. LowGrade cutaneous B-cell lymphoma in African American patients. Drugs Dermatol 2018;17:1334–7.

10. Lallas A, Apalla Z, Lefaki I, et  al. Dermoscopy of early stage mycosis fungoides. J Eur Acad Dermatol Venereol 2013;27:617–21. 11. Ozturk MK, Zindancı I, Zemheri E. Dermoscopy of stage IIA mycosis fungoides. North Clin Istanb 2019;7:174–9. 12. Geller S,  Rishpon A,  Myskowski PL. Dermoscopy in folliculotropic mycosis fungoides  – A  possible mimicker of follicle-based inflammatory and infectious disorders. J Am Acad Dermatol 2019;81:e75–e6. 13. Errichetti E, Piccirillo A, Stinco G. Dermoscopy as an auxiliary tool in the differentiation of the main types of erythroderma due to dermatological disorders. Int J Dermatol 2016;55:e616–e8. 14. Navarrete‐Dechent C, del Puerto C, Abarzúa‐Araya Á, et  al. Dermoscopy of primary cutaneous B‐ and T‐cell lymphomas and pseudolymphomas presenting as solitary nodules and tumours: A case‐control study with histopathologic correlation. Int J Dermatol 2019;58:1270–6. 15. Mascolo M, Piccolo V, Argenziano G, et  al. Dermoscopy pattern, histopathology and immunophenotype of primary cutaneous B-cell lymphoma presenting as a solitary skin nodule. Dermatology 2016;232:203–7. 16. Geller S, Navarrete‐Dechent C, Myskowski PL. Dermoscopy in lymphoproliferative disorders: Experience from a cutaneous lymphoma clinic in a tertiary cancer center. J Am Acad Dermatol 2019;80:e171–e2. 17. Apalla Z, Lallas A, Errichetti E. Lymphomas and pseudolymphomas. In: Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press, 2018:153–63.

8 Miscellaneous

Miscellaneous

Dermoscopy for skin of colour

Feroze Kaliyadan, Jayasree Puravoor, Balachandra Ankad, Richard Usatine, Aimilios Lallas, Bengu Nisa Akay, Nirmal Balakrishnan and Enzo Errichetti

8.1  Hailey-Hailey disease

8.1.3 Dermoscopy

8.1.1 Introduction

Dermoscopic examination of flexural lesions typically shows a white background (histologically related to epidermal thickening) along with reddish furrows (corresponding to superficial erosions) having a star-like, irregular, or, more frequently, linear shape (Figure 8.1B).1 Characteristically, such furrows are often parallel to each other, thus configuring a “tire tread-like” appearance (Figure  8.1B).1 Unlike in fair-skinned patients, vessels in skin of colour are difficult to appreciate.1 Lesions involving non-intertriginous areas are usually typified by linear, irregular, or star-like erosions (superficial loss of the epidermis due to acantholysis), as well as a reddish background, whitish scales and/or white/yellowish crusts (Figure  8.2B).1 White areas are generally not visible in such areas as they are associated with more vegetative lesions, typical of intertriginous and wet areas.1

Hailey-Hailey disease, also known as familial benign chronic pemphigus, is an autosomal dominant inherited dermatosis associated with mutations in the ATP2C1 gene (which encodes a calcium pump localized on the Golgi apparatus) that typically manifests in II–IV decades.1

8.1.2  Clinical presentation It manifests as short-lived vesicles/bullae on an erythematous background rapidly evolving into eroded, fissured and/ or crusted plaques or vegetations that mainly affect flexures (Figure 8.1A), yet extra-intertriginous areas may be involved (Figure 8.2A); single or multiple longitudinal white bands may also be seen on the nails.1

A

B

FIGURE 8.1  Hailey-Hailey disease (intertriginous lesion) in an African man (A). Dermoscopy reveals parallel linear erosions as well as white/yellowish scales/crusts (in the areas further from the axillary vault, which is more humid) (B). (From Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press.)

DOI: 10.1201/9780367816483-8

92

Miscellaneous A

B

FIGURE 8.2  Hailey-Hailey disease (non-intertriginous lesions) from the previous patient (A). Dermoscopic assessment displays linear and irregular erosions (arrows) associated with whitish scaling and white/yellowish crusts (B). (From Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press.)

8.2.3 Dermoscopy

8.2  Fixed drug eruption 8.2.1 Introduction Fixed drug eruption (FDE) is an adverse mucocutaneous drug reaction characterized by site-specific recurrence of lesions on systemic exposure to the inciting drug.2

8.2.2  Clinical presentation FDE presents as oval or round, dusky red macules or patches along with a burning sensation.2 Several morphological variants have been described, including vesicular, bullous, targetoid, erosive and generalized (Figure  8.3A).2 The lips (Figure  8.4A), genitalia, palms, soles and perineum are the most common involved sites.2 After subsidence of the acute phase, residual hyperpigmentation (which is particularly dark in skin of colour – Figure  8.3A) is the norm, yet a non-pigmenting variant has also been reported (which heals without leaving any trace).2

A

Inflammatory lesions usually feature just non-specific dermoscopic features, such as vessels, haemorrhages and/or purple background.3,4 Additionally, in mucosal involvement, erosions and white structureless areas may also be appreciated (Figure 8.4B).3,4 On the other hand, the pigmentary stage of FDE displays more characteristic features, namely diffuse coarse granular pigmentation typified by a mixed shade (i.e., grey-bluish as well as grey-brownish) and size (dots and globules) (Figure 8.3B).5 The variability in the colour results from the distribution of dermal pigment (free melanin and melanophages) at various levels in the dermis (i.e., superficial, mid and deep dermis). Finally, diffuse brown-grey pigmentation may also be observed (Figure 8.4B).5

B

FIGURE 8.3  Fixed drug eruption in an African man (A). Dermoscopy: brown to grey dots and globules with a variable shade and size throughout the lesion because of a different depth of pigment (free melanin/melanophages) in the dermis (B). (Courtesy of Arturo Galvan, MD – Verona, Italy.)

93

Dermoscopy for skin of colour A

B

FIGURE 8.4  Fixed drug eruption of the lower lip in a Middle Eastern man (A). Dermoscopic examination shows a central erosion surrounded by a white structureless rim; focal white structureless areas in the context of the erosion and multifocal brown-greys areas/dots are also evident (B).

8.3 Mastocytoses 8.3.1 Introduction The term mastocytosis encompasses a group of disorders typified by mast cell proliferation and accumulation in one or more organs, with the skin being the most commonly affected site.6 Three cutaneous forms are classically recognized, including maculopapular cutaneous mastocytosis (i.e., urticaria pigmentosa [UP] and telangiectasia macularis eruptiva perstans [TMEP]), diffuse cutaneous mastocytosis and mastocytoma.6 All the forms are quite rare in dark skin.7

8.3.2  Clinical presentation UP presents as more or less diffuse, red-brownish maculae, papules, nodules and/or plaques having various sizes (Figure  8.5A) (being larger and more infiltrated in children compared with adults); erythema and/or oedema may develop after scratching or rubbing (Darier’s sign).6,7 On the other hand, TMEP is typified by brownish-erythematous, 2–6 mm A

in diameter macules with irregular borders most commonly involving the chest and limbs.6,7 Diffuse cutaneous mastocytosis manifests as a diffuse leathery (pachydermatous) thickening of the skin displaying a “peau d’orange”, with or without nodular or blistering lesions, whereas mastocytoma is classically characterized by one or a few (up to five) brown nodules/plaques mainly involving the distal extremities (Figure 8.6A).6,7

8.3.3 Dermoscopy The main dermoscopic features of UP include homogeneous brown structureless areas or coarse pigment network (Figure  8.5B), whereas TMEP is mainly characterized by reticular vessels on an erythematous/brownish background (with or without brown network), although vessels may be difficult to appreciate in darker phototypes.6,7 When it comes to mastocytoma, dermoscopic examination typically reveals two main patterns, i.e., diffuse/multifocal yellow-orange areas (more infiltrated lesions) or brown background/reticular areas (Figure 8.6B).6,7 Notably, when the lesions are scratched and Darier’s sign develops, pigmentary structures become less visible on dermoscopy (Figure 8.5B).6,7

B

FIGURE 8.5  Urticaria pigmentosa in an Indian baby (A). Dermoscopy displays a coarse brown network; pigmentary structures become less visible after scratching the lesions (inset) (B).

94 A

Miscellaneous B

FIGURE 8.6  Mastocytoma in a Middle Eastern boy (A). Dermoscopic examination reveals a brown network (B).

8.4  Fordyce spots

8.5 Striae

8.4.1 Introduction Fordyce spots are ectopically located sebaceous glands not associated with hair follicles, with ducts that open directly to the skin surface.8,9

8.4.2  Clinical presentation They appear as multiple pinpoint white or yellowish papules most commonly affecting the vermillion border of the lips (Figure 8.7A), though the buccal and genital mucosa may also be involved.8,9 They are frequently noticed during puberty and tend to increase with age.8,9 No clear gender predilection has been noted so far.8,9

8.4.3 Dermoscopy Non-polarized dermoscopic assessment shows discrete and confluent yellowish globules, which appear shiny and white-yellow by using a polarized setting (Figure  8.7B).10 Additionally, branching linear vessels not crossing the globular structures may also be observed, especially on non-contact polarized dermoscopy (Figure 8.7B).10 Features of lesions on the penile shaft have been described as vascular “garlandslike” with “bows” that seem to wind around yellowish bunchlike lobules.10 Notably, in very dark phototypes, vessels are difficult to see.10

8.5.1 Introduction Striae (commonly called stretch marks) are a form of dermal scarring secondary to stress rupture of the connective tissue framework, as may happen in the case of stretched skin during pregnancy or sudden weight gain/loss.11,12

8.5.2  Clinical presentation The presentation of striae can vary according to the stage, with early lesions typified by thinned skin with mild erythema that progress to a more purplish colour (striae rubra) and finally become white and depressed (striae albae) (Figure  8.8A).11,12 The different colours are considered to be the outcome of a combination of vascular and pigmentary patterns.11,12

8.5.3 Dermoscopy Dermoscopy of striae rubra shows a faint violaceus background, along with linear vessels mainly arranged perpendicular to the long axis of the lesions, whereas striae albae are usually typified by reticulate brown lines distributed perpendicularly to the long axis (Figure 8.8B).11,12 The appearance is akin to the pigment network being stretched out, which probably corresponds to the loss of rete ridges.11,12

95

Dermoscopy for skin of colour A

B

FIGURE 8.7  Fordyce spots of the lips in a Middle Eastern man (A). Dermoscopy: discrete and confluent white-yellow globules and branching linear vessels not crossing the globular structures (B).

A

B

FIGURE 8.8  Striae albae in a Middle Eastern boy (A) that feature reticulate brown lines distributed perpendicularly to the long axis on dermoscopy (B).

8.6  Keratolysis exfoliative 8.6.1 Introduction Keratolysis exfoliative is a benign dermatosis of the volar skin of the hands and feet that is thought to be related to a premature corneo-desmosomal disruption.13

8.6.2  Clinical presentation It manifests as asymptomatic, superficial air-filled blisters on a mildly erythematous base that then proceed to superficial exfoliative scaling (Figure 8.9A).13

8.6.3 Dermoscopy Dermoscopy features of keratolysis exfoliative include superficial white scales arranged in a peripheral arciform or annular pattern, although they may present a diffuse distribution pattern (Figure 8.9B); in this last case the ridges tend to be seen over the scale (Figure 8.9B) (authors’ personal observations).

96 A

Miscellaneous B

FIGURE 8.9  Keratolysis exfoliative in a Middle Eastern man (A). Dermoscopy: superficial white scales arranged in a peripheral arciform pattern and diffuse pattern with scales located over the ridges (B).

8.7  Nevus comedonicus 8.7.1 Introduction Nevus comedonicus is an uncommon hamartoma of the pilosebaceous unit that belongs to the spectrum of epidermal nevi.14,15

8.7.2  Clinical presentation It is clinically characterized by dilated comedo-like openings, with black or brown keratin plugs most frequently involving the face, neck, upper arms, chest, or abdomen (Figure 8.10A).14,15

A

Lesions can be present at birth or develop in early childhood, arranged in groups or follow a linear pattern along the Blaschko lines.14,15

8.7.3 Dermoscopy Non-polarized dermoscopy shows discrete brown and black globular areas that are slightly elevated from the surface.14,16 Such structures appear as round/ovoidal brown-black globules surrounded by circular and barrel shaped areas of varying shades of hyperpigmentation under polarized light (Figure  8.10B).14,16 Histologically, the globules correspond to keratin plugs mixed with melanin.14,16

B

FIGURE 8.10  Nevus comedonicus in a Middle Eastern boy (A). Dermoscopic examination displays round/ovoidal brown-black globules surrounded by circular brown pigmentation (B).

97

Dermoscopy for skin of colour A

B

FIGURE 8.11  Small-vessels vasculitis in a North African male (A). Dermoscopy: violaceous blurred purpuric spots/blotches arranged in a mottled/ speckled pattern and blue-grey patches (B).

8.8  Cutaneous vasculitis

necrotic crusts surrounded by purple areas are further possible findings.1

8.8.1 Introduction The term “vasculitis” encompasses a group of conditions characterized by inflammation of the blood vessel walls.1 Based on the size of the affected blood vessels, they are classified into three groups, namely small-vessels, medium-vessels and largevessels vasculitis, with the first two types often displaying skin involvement.1

8.8.2  Clinical presentation Small-vessels vasculitis typically presents as purpuric macules and papules (Figure 8.11A) that may sometimes be associated with haemorrhagic vesicles/blisters, inflammatory papules, urticarial plaques and/or skin necrotic areas.1 Broken livedo, skin infarctions, ulcerations and deep nodules are characteristic of medium-vessels vasculitis.1 Postinflammatory pigmentary changes are frequent in dark skin.1

8.8.3 Dermoscopy Dermoscopy is mainly used to evaluate the purpuric lesions of small-vessels vasculitis.1 In particular, they typically feature violaceous blurred purpuric spots/blotches often arranged in a mottled/speckled pattern (Figure  8.11B), histologically corresponding to extravasated erythrocytes and perivascular inflammation.1 Additionally, blue-grey patches resulting from dermal vascular injury/extravasated erythrocytes may also be observed and have been reported to be quite characteristic of small-vessels vasculitis (Figure 8.11B).1 Ulceration/ erosions, haemorrhagic vesicles/blisters and haemorrhagic/

8.9  Pigmented purpuric dermatoses 8.9.1 Introduction Pigmented purpuric dermatoses (PPDs), also referred to as capillaritis, include several chronic conditions typified by erythrocytes extravasation in the skin, with consequent hemosiderin deposits.1 They have been related to venous stasis or reactive responses to external triggers.1

8.9.2  Clinical presentation Five main clinical subtypes of PPDs are classically recognized, including Schamberg disease (brown/coppery-coloured macules/patches with pinpoint petechiae) (Figures 8.12A and 8.13A), Doucas–Kapetanakis disease (similar to the previous one with the addition of eczematous lesions), Majocchi’s disease (annular reddish patches with subtle telangiectasias and pinpoint purpuric spots), Gougerot–Blum syndrome (association of dark papules along with pinpoint purpuric spots) and lichen aureus (one or few “golden-coloured” patches containing purpuric spots).1

8.9.3 Dermoscopy All the variants of PPDs are typified by round to oval, purpuric dots and/or globules (histologically corresponding to extravasated erythrocytes in the dermis), commonly located over a brownish to coppery background (resulting from

98

Miscellaneous

dermal hemosiderin deposits) (Figure  8.12B).1 Notably, in dark-skinned patients, the purpuric spots are usually less evident/numerous compared with those in fair-skinned subjects and are often associated with a brown network (Figure  8.12B) resulting from basal layer hyperpigmentation, which may be sometimes the only dermoscopic feature

A

in long-standing cases (Figure  8.13B) (authors’ personal observations). Additional dermoscopic features include brownish dots/ globules (corresponding to dermal pigment incontinence), telangiectatic vessels (Majocchi disease) and yellowish scaling and/or crusts (Doucas–Kapetanakis disease).1

B

FIGURE 8.12  Schamberg disease in a North African male (A). Dermoscopy: a few purpuric dots located over a brownish to coppery background; brown networks resulting from basal layer hyperpigmentation are also seen (B).

A

B

FIGURE 8.13  Long-standing Schamber disease in an Indian man (A). Dermoscopy shows only a brown network with no purpuric spot (B).

99

Dermoscopy for skin of colour

8.10  Cutaneous xanthomas 8.10.1 Introduction Cutaneous xanthomas are lipid deposits present in the dermis and/or subcutaneous layer.17–20 These are considered as symptoms of various lipoprotein disorders, rather than a disease. 17–20 All the xanthoma lesions show the presence of foam cells (macrophages loaded with lipids).17–20

8.10.2  Clinical presentation Several clinical forms of xanthomas are recognized, namely tendon xanthoma (subcutaneous nodules mainly present in the Achilles tendon and over the knuckles – associated with familial and secondary hypercholesterolemia), tuberous xanthoma (firm yellowish-reddish nodules mainly involving the extensor surface of the elbows and knees, buttocks and heels  – associated with type III hyperlipoproteinaemia) (Figure  8.14A), eruptive xanthoma (2–5  mm in diameter, yellow-red papules occurring on extensor surfaces  – associated with any cause

A

of hypertriglyceridemia) (Figure 8.15A) and plane xanthomas (i.e., xanthelasma, plane xanthoma and palmar xanthoma  – associated with familial hypercholesterolemia, type III hyperlipoproteinemia and chronic cholestasis) (Figure 8.16A).17–20

8.10.3 Dermoscopy All the forms of cutaneous xanthomas are typically characterized by the presence of yellow structureless areas, lines or globules (Figures  8.14B–8.16B), which histologically correspond to accumulation of macrophages loaded with lipids (foam cells) in the dermis or subcutaneous tissues, along with distorted pigment network.1 The shade of yellow structures may vary according to the depth of the lipid deposits, with superficial and deep lesions being respectively characterized by bright yellow and brownish hues (Figures  8.14B–8.16B).1 Notably, in the context of the same lesion, the shade of yellow areas often varies because of the presence of lipids deposits at different levels.1 Vessels (linear-curved or linear-branched) may sometimes be appreciated (Figures  8.15B and 8.16B), especially in plane and eruptive xanthomas.1

B

FIGURE 8.14  Tuberous xanthoma in an Indian boy (A). Dermoscopic assessment reveals yellow to brownish lines and globules (B).

A

B

FIGURE 8.15  Eruptive xanthoma in an Indian man (A). Dermoscopy: bright yellow structureless background along with linear-curved vessels and peripheral reddish halo (B).

100

Miscellaneous A

B

FIGURE 8.16  Plane xanthoma of the neck in an Asian male (A). Dermoscopy: bright yellow structureless areas and linear-branching vessels (B).

8.11 Xanthogranuloma 8.11.1 Introduction Xanthogranuloma is a benign cutaneous condition belonging to the broad group of non-Langerhans cell histiocytosis.6 Even though it commonly presents during infancy, adult-age onset is not so rare.6 Such a disease usually disappears spontaneously over a period of 3–6  years, yet a chronic course is possible, especially in adults.6

8.11.2  Clinical presentation Xanthogranuloma in dark-skinned patients manifests as one or more asymptomatic, discrete, skin-coloured or redbrown papules and/or nodules progressively turning yellowish, which mainly affect the upper part of the body and arms (Figures  8.17A–8.19A).6 Extracutaneous involvement is rare, with the eye being the most commonly affected site.6

A

8.11.3 Dermoscopy The main dermoscopic feature of xanthogranuloma is represented by diffusely or focally distributed orange and/or yellow areas (Figures  8.17B–8.19B), which are histologically related to the dense cellular infiltration by histiocytes (“mass effect” – responsible for the orange shade) and foamy lipid-laden cells (responsible for the yellow shade) in the dermis.6 Importantly, although yellow structures are considered quite characteristic of dermatoses characterized by lipid deposits (histiocytoses and xanthomas), they may also be seen in other conditions (e.g., thyroglossal duct cyst) (Figure 8.20), but the presence of a multiglobular pattern (corresponding to focal aggregates of lipidized cells) is rather indicative of histiocytoses and xanthomas.6 Central sharp branching vessels and a peripheral erythematous halo (giving rise to the so-called “setting sun” pattern when it is associated with a central orangish-yellowish area) may also be seen, yet they are less frequent in skin of colour.6 Additionally, pigmentary structures (e.g., structureless brown areas or network) are often seen in dark-skinned patients (Figures 8.17B–8.19B).6

B

FIGURE 8.17  Multiple xanthogranulomas in an Asian man (A). Dermoscopic assessment reveals multifocal orange-yellow areas and structureless brown areas (B).

101

Dermoscopy for skin of colour A

B

FIGURE 8.18  Juvenile xanthogranuloma in an African American boy (A). Dermoscopy displays a yellow background and peripheral brown pigmentation (B).

A

B

FIGURE 8.19  Hyperkeratotic juvenile xanthogranuloma in a Hispanic boy (A). Dermoscopy displays multiglobular yellow areas, white scaling and multifocal brown pigmentation (B).

A

B

FIGURE 8.20  Thyroglossal duct cyst in an African boy (A). Dermoscopy: diffuse yellow background and focal brown pigmentation (B).

102

Miscellaneous

8.12.3 Dermoscopy

8.12  Prayer nodules 8.12.1 Introduction Prayer nodules are relatively common lesions in response to prolonged and repetitive trauma to the skin encountered in people who pray regularly.21

8.12.2  Clinical presentation They present as lichenified, crusted and/or haemorrhagic nodules/plaques (Figure  8.21A) or hyperpigmented nodules (Figures  8.22A and 8.23A) most commonly involving the forehead, knees, ankles and dorsum of the feet.21 Localization depends on the adopted position for meditation.21

A

Dermoscopy typically shows white thick hyperkeratosis that sometimes may display a cracked appearance (Figure 8.21B). Generally, unlike lichen simplex chronicus, there are no or few vessels (generally linear or dotted). Additionally, hyperpigmented variants usually display just little white scales and parallel brown dots/lines over a brownish background (Figures  8.22B and 8.23B) histologically corresponding to basal layer hyperpigmentation (authors’ personal observations).21 Follicular plugs may also be observed, similarly to discoid lupus erythematosus, yet the presence of linear pigmented structures may help in differentiation (Figure 8.23B).

B

FIGURE 8.21  Prayer nodule of the dorsum of the left foot in a North African man (A). Dermoscopic examination shows thick hyperkeratosis displaying a cracked appearance (B).

A

B

FIGURE 8.22  Pigmented prayer nodule of the forehead in an Asian man (A). Dermoscopy: little white scales and parallel brown dots/lines over a brownish background (B).

103

Dermoscopy for skin of colour A

B

FIGURE 8.23  Pigmented and lichenified prayer nodule of the forehead in a North African man (A). Dermoscopy: brown background, sparse dotted vessels, follicular plugs and brown lines (arrow in the inset) (B).

8.13  Cutaneous mucinoses 8.13.1 Introduction Cutaneous mucinoses include a wide group of conditions characterized by an abnormal mucin deposition in the skin.6 They are classified into two groups, i.e., primary (idiopathic) cutaneous mucinoses (mucin deposit is the main histological feature) and secondary mucinoses (mucin deposit is a secondary phenomenon).6 The former is further divided into dermal and follicular mucinoses, both of them including various subtypes, with the most common form being lichen myxedematous (papular mucinosis).6

8.13.2  Clinical presentation Dermal mucinoses (papular lichen myxedematosus, nodular lichen myxedematosus, obesity-associated lymphoedematous mucinosis, scleromyxedema, scleredema, connective tissue diseases-associated mucinosis, acral persistent papular mucinosis, pretibial myxoedema, cutaneous papular mucinosis of infancy and self-healing cutaneous mucinosis) manifest as asymptomatic, dome-shaped or flat-topped whitish/skincoloured papules, nodules and/or plaques, which may be diffuse (scleromyxedema) or more or less localized (other forms) (Figure  8.24A).6 Sclerodermoid changes (Figure  8.25A), diffuse infiltration of the glabella (leonine face) and skin overlying the dorsal aspect of proximal interphalangeal joints (“doughnut” sign) (Figure  8.26A) and linear arrangement of the papules are also often seen in scleromyxedema.6 Follicular mucinoses present as one or several sharply demarcated erythematous plaques, often with scaling and

alopecia; nodules, annular plaques, folliculitis-like lesions, follicular spines, acne-like eruptions and alopecia areata-like presentation have also been described.6 Additionally, urticarialike follicular mucinosis presents with recurrent pruritic urticarial papules and plaques of the face and neck.6 Other variants of skin mucinosis include cutaneous focal mucinosis, digital myxoid cysts and reticular erythematous mucinosis.6

8.13.3 Dermoscopy Dermoscopy of dermal mucinoses mainly shows white (often bright) areas (Figures  8.24B–8.26B), which may be diffuse, globular, or linear, that are histologically related to dermal mucin deposits along with dermal oedema (especially diffuse white areas) and/or dermal fibrosis (especially globular and linear white structures).6 Moreover, scleromyxedema, generalized myxoedema, scleredema and localized pretibial myxoedema commonly feature dilated follicular openings too.6 Of note, in dark skin, white areas usually are devoid of pigment remnants apart from a peculiar perifollicular sparing that may sometimes be seen (Figure 8.25B) (authors’ personal observations). Some peculiarities may be associated with specific clinical subtypes, including broken hairs and alopecic areas in scleromyxedema, haemorrhagic spots and/or brown to rust-coloured areas (due to hemosiderin deposits) in obesity-associated lymphoedematous mucinosis, pigmentary structures in both localized pretibial myxoedema and cutaneous focal mucinosis and dotted and linear irregular vessels in reticular erythematous mucinosis.6 Follicular mucinosis usually reveals dilated follicular openings devoid of hairs (histologically resulting from mucin accumulation within the follicular epithelium with its consequent enlargement), which are often filled with keratotic material.6

104

Miscellaneous A

B

FIGURE 8.24  Discrete papular lichen myxedematous in an African man (A). Dermoscopy reveals bright white roundish areas (B). (From Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press.)

A

B

FIGURE 8.25  Scleromyxedema in an Indian man with sclerodermoid changes of the back causing deep furrows (“Shar-pei” sign) (A). Dermoscopy: white areas devoid of pigment remnants, except for a peculiar perifollicular sparing (B).

A

B

FIGURE 8.26  Sclerodermoid changes of the dorsal aspect of the left hand with depigmentation and the so-called “doughnut” sign overlying the proximal interphalangeal joints in the previous patient (A). Dermoscopy: white areas with absence of physiological pigmentation (B).

105

Dermoscopy for skin of colour

8.14  Ichthyosis vulgaris and X-linked ichthyosis 8.14.1 Introduction Ichthyosis vulgaris and X-linked ichthyosis are the most common forms of inherited ichthyosis, having a prevalence of 1:250/1:1000 and 1:2000/1:6000, respectively.22 The former follows an autosomal dominant inheritance and is associated with mutations in the gene encoding filaggrin, whereas the latter mainly affects males and is caused by a mutation of the enzyme steroid sulfatase.22

8.14.2  Clinical presentation Both ichthyosis vulgaris (Figure 8.27A) and X-linked ichthyosis (Figure 8.28A) typically present as skin desquamation that generally improves during summertime.22 However, scales in

A

the latter are usually coarser and darker, occur earlier (usually in the first 3 months vs during the first 3–12 months) and, unlike ichthyosis vulgaris, often involve the flexures (especially the neck).22

8.14.3 Dermoscopy Dermoscopy of ichthyosis vulgaris typically shows roundish or polycyclic white scales with an inner free edge (Figure 8.27B), whereas thick, light to dark brown, roundish or polygonal scales are seen in X-linked ichthyosis (Figure 8.28B) (authors’ personal observations). Such a difference is because of the different histological background as only the latter form displays a thickened granular layer, which is responsible for a thicker and darker scaling, whereas ichthyosis vulgaris generally shows a normal or diminished granular layer (authors’ personal observations).

B

FIGURE 8.27  Ichthyosis vulgaris of the legs in an African man (A). Dermoscopic examination displays roundish and polycyclic white scales with an inner free edge (B).

A

B

FIGURE 8.28  X-linked ichthyosis of the legs in an African boy (A) Dermoscopy reveals thick, light to dark brown, roundish and polygonal scales (B).

106

Miscellaneous

8.15  Granular parakeratosis 8.15.1 Introduction Granular parakeratosis is an uncommon benign skin condition typified by a distinctive histological reactive pattern, i.e., granular appearance of the parakeratotic horny layer.23 It is thought to be a reactive condition to external stimuli (e.g., antiperspirants) possibly interfering with the maturation of the stratum granulosum and stratum corneum, yet some authors think that it may represent a disorder of cornification.23

8.15.2  Clinical presentation From a clinical point of view, granular parakeratosis manifests as unilateral/bilateral, grouped, red-brown (even dark A

brown/black in dark skin), scaly, crusted, hyperkeratotic papules often coalescing into plaques mainly affecting the armpits (Figure 8.29A) or other folds, though extra-intertriginous areas may be involved.23 Lesions are usually asymptomatic, yet pruritus or pain may be present.23

8.15.3 Dermoscopy Dermoscopic examination of granular parakeratosis in darkskinned patients may show an intensely pigmented background presenting as a black/brown network or structureless areas (histologically corresponding to basal layer hyperpigmentation) along with white scales (related to hyperkeratosis) and white structureless areas containing brighter globules/ areas (resulting from acanthosis – white background – and foci of compact parakeratosis with retention of basophilic keratohyalin granules  – brighter globules/areas) (authors’ personal observations) (Figure 8.29B). B

FIGURE 8.29  Granular parakeratosis of the armpit in an African American man (A). Dermoscopic examination shows an intensely pigmented background presenting as black/brown structureless areas, with white scales, and white structureless areas containing brighter globules/areas (B).

REFERENCES 1. Errichetti E, Lallas A. Miscellaneous inflammatory diseases. In: Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press, 2018:130–51. 2. Sehgal VN, Srivastava G. Fixed drug eruption (FDE): Changing scenario of incriminating drugs. Int J Dermatol 2006;45:897–908. 3. Nayak SS, Mehta HH, Gajjar PC, Nimbark VN. Dermoscopy of general dermatological conditions in Indian population: A descriptive study. Clin Dermatol Rev 2017;1:41–51. 4. Valdebran M, Salinas RI, Ramirez N, et al: Fixed drug eruption of the eyelids. A  dermoscopic evaluation. Our Dermatol Online 2013;4:344–6. 5. Errichetti E, Lallas A. Hyperpigmented dermatoses. In: Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press, 2018:106–20. 6. Errichetti E, Lallas A. Other infiltrative conditions. In: Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press, 2018:173–7.

7. Nirmal B, Krishnaram AS, Muthu Y, Rajagopal P. Dermatoscopy of urticaria pigmentosa with and without Darier’s sign in skin of colour. Indian Dermatol Online J 2019;10:577–9. 8. Lee JH, Lee JH, Kwon NH, et al. Clinicopathologic manifestations of patients with Fordyce’s spots. Ann Dermatol 2012;24:103–6. 9. Saha A, Bandyopadhyay D. Fordyce’s spots. Indian Pediatr 2015;52:266. 10. Micali G, Lacarrubba F. Augmented diagnostic capability using videodermatoscopy on selected infectious and noninfectious penile growths. Int J Dermatol 2011;50:1501–5. 11. Kaliyadan F,  Jha AK,  Sonthalia S. Dermoscopy  of  striae  rubrae. Indian Dermatol Online J 2018;9:477–8. 12. Hermanns JF, Piérard GE. High-resolution epiluminescence colourimetry of striae distensae.  J Eur Acad Dermatol Venereol 2006;20:282–7. 13. Hausauer AK, Cohen DE. Keratolysis exfoliativa. Dermatol Online J 2015;21:13030. 14. Špiewak R, Winciorek G. Dermoscopy on nevus comedonicus: A case report and review of the literature. Postep Derm Alergol 2013;4:252–4.

107

Dermoscopy for skin of colour 15. Vano-Galvan S, Hernandez-Martin A. Disseminated congenital comedones. Pediatr Dermatol 2011;28:58–9. 16. Vora RV, Kota RS, Sheth NK. Dermoscopy of nevus comedonicus. Indian Dermatol Online J 2017;8:388–9. 17. Flynn PD. Xanthomas and abnormalities of lipid metabolism and storage. In: Rook’s textbook of dermatology (Burns T, Breathnach S, Cox N, Griffiths C, eds.), 8th edn. Malden: Blackwell. 2010:62.1. 18. Shah AC, Shah MM, Mahajan RS, Bilimoria FE. Eruptive xanthoma: A rare cutaneous marker of secondary hyperlipidemia. J Integr Health Sci 2014;2:40–1. 19. Mohan KK, Kumar KD, Ramchandra BV. Tuberous xanthomas in type IIA hyperlipoproteinemia. Indian J Dermatol Venereol Leprol 2002;68:105–6.

20. Nair PA, Singhal R. Xanthelesma palpebrarum- a brief review. Clin Cosmet Investig Dermatol 2018;11:1–5. 21. Rehman H, Asfour NA. Clinical images: Prayer nodules. CMAJ 2010;182:E19. 22. Judge MR, McLean WHI, Munro s. Disorders of keratinization. In: Rook’s Textbook of Dermatology (Griffiths CEM, Barker J, Bleiker T, Chalmers R, Creamer D, eds), 9th ed. Oxford: Wiley-Blackwell. 2016:19.1–60. 23. Ding CY, Liu H, Khachemoune A. Granular parakeratosis: A  comprehensive review and a critical reappraisal. Am J Clin Dermatol 2015;16:495–500.     F

Part II

Infectious Diseases

9 Bacterial infections

Bacterial infections

Dermoscopy for skin of colour

Balachandra Ankad, Vinay Keshavamurthy, Shekhar Neema, Payal Chauhan and Enzo Errichetti

9.1 Leprosy 9.1.1 Introduction Leprosy, also known as Hansen’s disease, is a chronic granulomatous disease caused by Mycobacterium leprae that typically affects the skin, mucous membranes (e.g., nose), peripheral nervous system, eyes and testes.1,2 Several disease phenotypes are possible based on the patient’s immunity, with more severe forms occurring in subjects with a less effective immune response to the infection.1,2

9.1.2  Clinical presentation The main clinical subtypes of leprosy include indeterminate, tuberculoid, borderline tuberculoid, borderline borderline, borderline lepromatous and lepromatous leprosy; lepra bonita (diffuse skin infiltration) and histoid leprosy are rarer forms.1,2 During the course of the infection, immunologically mediated episodes of acute or subacute inflammation known as “lepra reactions” (type 1 and type 2) may occur.1,2 Tuberculoid leprosy (Figure  9.1A) presents with single or multiple, asymmetric, well-defined, erythematous plaques with raised and clear-cut edges sloping inward and a dry, anaesthetic and hairless surface, with or without scales.1,2 Lesions can flatten over time with hypochromic centre. It is associated generally with solitary nerve thickening.1,2 Borderline tuberculoid leprosy (Figures  9.2A and 9.3A) is similar to tuberculoid leprosy, yet the size of the lesion is larger, number of lesions is greater, margins may be both well- or ill-defined, and loss of sensation and dryness is usually less marked; satellite lesions may also be present (Figure 9.3A).1,2 Borderline borderline leprosy (Figure  9.4A) is a very unstable variant that is typified by multiple lesions having various shapes and sizes (papules, nodules, plaques and circinate lesions); punched out with “Swiss cheese” appearance lesions and plaques featuring an indistinct outer border and well-defined inner border with hypopigmented centre are suggestive of this clinical variant.1,2 Many nerves are involved but neurological deficit is scant until the reaction sets in.1,2 Borderline lepromatous leprosy (Figure  9.5A) manifests as multiple, ill-defined, round macules with coppery hue that then evolve into infiltrated lesions (i.e., papules, plaques and nodules); distribution is central rather than peripheral and lacks symmetry. Sensations and hair growth in the lesions are slightly diminished and partial loss of the eyebrows can

be seen, whereas the peripheral nerves get involved leading to anaesthesia and paresis.1,2 Lepromatous leprosy (Figure  9.6A) in the early phases shows widely disseminated and symmetric erythematous or hypochromic macules that progress into nodules and plaques with borders merged into the normal skin; the lesions are not anaesthetic and do not show any change in skin texture, hair growth or sweating. The peripheral nerves become thickened, firm and fibrosed, and internal organs may be affected.1,2 Histoid leprosy (Figure  9.7A) is a variant of lepromatous leprosy presenting with shiny, hemispherical, dome-shaped, non-tender and soft to firm nodules mainly distributed over bony prominences. Interestingly, hypopigmented patches are not seen in this type of leprosy.1,2 Type 1 lepra reaction (Figure  9.8A) is characterized by the development of acute inflammation in skin lesions and/or nerves; pre-existing cutaneous lesions become redder, shiny, prominent, swollen, warm and tender, thus resemble erysipelas; borderline leprosy is a strong risk factor for this type of reaction.1–4 Type 2 lepra reaction (Figure 9.9A) is because of humoral immunity exclusively seen in lepromatous leprosy and, sometimes, in borderline lepromatous leprosy that presents with painful and evanescent erythematous nodules (erythema nodosum leprosum); no changes in pre-existing lesions are seen.1–4

9.1.3 Dermoscopy Tuberculoid (Figure 9.1B), borderline tuberculoid (Figures 9.2B and 9.3B) and borderline borderline (Figure 9.4B) leprosy share similar dermoscopic patterns, consisting of a diminished distorted pigment network along with focal or diffuse dull white structureless areas (corresponding to a decreased number of melanocytes) and a decreased number of white dots and hair follicles as compared with normal skin (because of the tropism of inflammatory infiltrate for skin appendages), with the last feature being the most characterizing one.2,5,6 Additionally, hair changes (i.e., broken hairs, coiled hairs and, rarely, V-like hairs), widened skin furrows, brown-yellow/ orange globules (histologically related to granulomas) and focused linear, dotted/globular and branching vessels (resulting from dermal vessels dilatation) may also be seen in skin of colour.2,5,6 Such dermoscopic features are mainly seen on facial lesions (especially vessels because of the richer vascularity) and infiltrated extra-facial lesions.2,5,6 On the other hand, in borderline lepromatous (Figure 9.5B) and lepromatous leprosy (Figure  9.6B), brown-yellow/orange DOI: 10.1201/9780367816483-9

112 globules are usually not well-appreciated or are absent because of the lack of compact granulomas, whereas white bright lines resulting from dermal fibrosis are often seen.2,5,6 As observed in other forms of leprosy, it is possible to see a diminished distorted pigment network, focal or diffuse dull white structureless areas and a decreased number of appendages.2,5,6 Histoid leprosy (Figure  9.7B) features brown-yellow globules (histologically corresponding to the dense dermal infiltration by macrophage) along with linear, branching and globular vessels as well as white lines and/or structureless areas (related to the pronounced dermal fibrosis); a perilesional pigment network (due to basal layer hyperpigmentation) is also often seen.7 The main dermoscopic features related to type 1 lepra reaction (Figure 9.8B) include pronounced vessels of mixed

A

Bacterial infections morphology (i.e., linear, red and milky globular and dotted) related to the marked inflammation with the heavy lymphocytic infiltration typical of such a reaction.2 Brown-yellow globules become less evident because of dermal oedema whereas broken hairs (black dots – related to partial follicular damage by inflammatory infiltrate) and white scaling (histologically corresponding to hyperkeratosis) are conspicuously seen.2 In type 2 lepra reaction (Figure  9.9B), it is possible to appreciate characteristic milky-red structureless areas that are more pronounced than that of type 1 reaction, whereas granulomas appear as reddish-brown areas rather than brownish-yellow globules and no scales or follicular changes are observed.2

B

FIGURE 9.1  Clinical image of tuberculoid leprosy in an Indian man shows a well-defined plaque above the eyebrow (box indicates the site of dermoscopic examination) (A). Dermoscopy: brownish-orangish multifocal structureless areas, focused linear-branching vessels and decreased number of white dots (eccrine glands openings) (B).

A

B

FIGURE 9.2  Clinical image of borderline tuberculoid leprosy in an Indian woman reveals well-defined slightly erythematous plaques of the left side of the face (arrows) (A). Dermoscopic examination displays ill-defined dull white areas along with diminished distorted pigment network and decreased number of white dots as compared with normal skin (B).

113

Dermoscopy for skin of colour A

B

FIGURE 9.3  Clinical image of borderline tuberculoid leprosy on the dorsum of the right hand in an Indian woman shows a well-defined plaque with satellite lesions (arrow) (A). Dermoscopy: multifocal ill-defined dull white areas, diminished distorted pigment network, widened skin furrows and reduction of white dots and hairs (B).

A

B

FIGURE 9.4  Clinical image of borderline borderline leprosy in an Indian boy displays multiple ill- to well-defined annular and geographic plaques on the trunk (A). Dermoscopy: diminished distorted pigment network along with pinkish globules (B).

A

B

FIGURE 9.5  Clinical image of borderline lepromatous leprosy in an Indian man reveals multiple ill- to well-defined coppery red and hypopigmented patches and macules in a symmetrical fashion on the legs (A). Dermoscopy: multifocal ill-defined white areas and diminished distorted pigment network along with widened skin furrows and reduction of white dots (B).

114 A

Bacterial infections B

FIGURE 9.6  Clinical image of lepromatous leprosy in an Indian man shows multiple erythematous plaques and nodules in a symmetrical fashion on the trunk (A). Dermoscopy: white bright lines over a white background along with lack of pigment network and appendages (B).

A

B

FIGURE 9.7  Clinical image of histoid leprosy in an Indian woman reveals multiple cutaneous and subcutaneous nodules on the foot and leg (A). Dermoscopic assessment displays globular, linear and branching vessels along with brownish-yellow structureless areas, whitish-pink background and a perilesional pigment network (B).

A

B

FIGURE 9.8  Clinical image of borderline tuberculoid leprosy with type 1 reaction in an Indian man displays multiple erythematous and indurated plaques with slight scaling (A). Dermoscopy: ill-defined white areas with diminished distorted pigment network, patchy white scaling, vessels of mixed morphology (linear-irregular and dotted) and erythema (B).

115

Dermoscopy for skin of colour A

B

FIGURE 9.9  Clinical image of lepromatous leprosy with erythema nodosum leprosum in type 2 lepra reaction in an Indian woman: erythematous subcutaneous nodules on the trunk (A). Dermoscopy: milky red globules/areas, multifocal white areas and reddish-brownish globules (arrow) (B).

9.2  Cutaneous tuberculosis 9.2.1 Introduction Lupus vulgaris and tuberculosis verrucosa cutis are the most frequent clinical variants of cutaneous tuberculosis, a skin infection mainly caused by Mycobacterium tuberculosis.8 The former results from a reinfection by exogenous inoculation or internal spread, whereas the latter is a primary infection due to a direct inoculation into the skin.8 Besides the previously mentioned variants of skin tuberculosis, it is noteworthy to mention a relatively common form of tuberculid (skin manifestations occurring as a reaction to hematogenous spread of Mycobacterium tuberculosis), viz. lichen scrofulosorum, which mainly affects children and young adults.9,10

9.2.2  Clinical presentation Lupus vulgaris (Figure 9.10A) typically manifests as discrete, red-brown papules that gradually coalesce into large, asymptomatic plaques with central resolution and/or atrophy; the head and neck area is the most common site of involvement, yet the lower extremities or buttocks are the most frequent sites in subtropical and tropical areas.2,8 On the other hand, tuberculosis verrucosa cutis (Figure 9.11A) presents as a brown-red warty nodule or plaque usually affecting the extremities, especially the hands and feet.2,8 Finally, lichen scrofulosorum presents as asymptomatic, skin-coloured to reddish-brown, follicular and perifollicular, grouped papules with slight scaling that occurs over the trunk and proximal extremities (Figure 9.12A); the lesions can also coalesce to from discoid or annular plaques.9,10

9.2.3 Dermoscopy The dermoscopic pattern of lupus vulgaris is similar to that of other granulomatous dermatoses (especially skin sarcoidosis), being mainly characterized by focal or diffuse orange-yellow structureless areas histologically corresponding to dermal granulomas (Figure  9.10B).2,11 Notably, in very dark phototypes, such areas have a yellower hue because of the presence of an intensely pigmented background (Figure 9.10B).2,11 Additionally, even though in fairskinned patients lupus v ­ulgaris and sarcoidosis are hard to differentiate on dermoscopy, in skin of colour there is a significantly higher ­prevalence of white structureless areas in the former because of a more pronounced dermal fibrosis (Figure 9.10B).2,11 Focused linear/linear-branched vessels may also be seen.2,11 On the other hand, orange-yellow structureless areas are observed less commonly in tuberculosis verrucosa cutis as they are covered by the overlying acanthosis and hyperkeratosis, which are responsible for a white background and white scaling, respectively (Figure  9.11B) (authors’ personal observations). Additionally, more or less diffuse dotted vessels and bright white areas are also frequently observed because of dilated vessels in elongated dermal papillae and dermal fibrosis, respectively (Figure 9.11B) (authors’ personal observations). Lichen scrofulosorum is typified by round, perifollicular pale-white dots (histologically related superficial upper dermal granulomas centred around hair follicles and eccrine glands) surrounded by a rim of pigmentation and erythematous areas; follicular plugs, fine scaling and vessels may also be appreciated (Figure 9.12B).12

116 A

Bacterial infections B

FIGURE 9.10  Lupus vulgaris of the left armpit in an Indian woman (A). Dermoscopy shows bright white structureless areas, multifocal yellow structureless areas and patchy white scales (B).

A

B

FIGURE 9.11  Tuberculosis verrucosa cutis of the foot in an Indian woman (A). Dermoscopic examination displays white background, white scaling and patchy dotted vessels (B).

A

B

FIGURE 9.12  Lichen scrofulosorum in an Indian child. Clinical appearance (A). Dermoscopy reveals multiple, perifollicular, round, pale-white dots surrounded by a rim of pigmentation, erythema and few vessels; follicular plugs and fine scaling also appreciated (B).

117

Dermoscopy for skin of colour

9.3.3 Dermoscopy

9.3  Impetigo and ecthyma simplex 9.3.1 Introduction Impetigo (bullous and non-bullous) and ecthyma are two of the most common bacterial cutaneous infections in dark-skinned patients, with the former mainly involving the superficial layers of the epidermis and the latter extending to both the deep epidermis and dermis.13,14 Whereas in industrialized countries Staphylococcus aureus is the main causal agent of non-bullous impetigo, in developing nations this infection is often due to Streptococcus pyogenes, which is also responsible for most cases of ecthyma.13,14 On the other hand, bullous impetigo is caused almost exclusively by S. aureus producing exfoliative toxins at the infection sites.13,14

9.3.2  Clinical presentation Non-bullous impetigo is characterized by small superficial pustules or blisters that quickly rupture and evolve into one or more honey-coloured or brownish (especially in darker phototypes), polycyclic, crusted plaques mainly occurring on the face of children.13,14 Bullous impetigo is also typical of this age span but more commonly involves intertriginous areas and presents with localized superficial, aflegmasic, flaccid bullae containing a cloudy/yellow fluid that rupture easily to form honey-coloured or brownish, roundish, crusted plaques (Figures 9.13A and 9.15A).13,14 Finally, ecthyma presents with punched-out skin ulcerations covered with a thick brownish adherent crust, which may be surrounded by an erythematous halo (with the exception of phototypes V/VI) (Figure  9.16A).13,14 Differently from impetigo, ecthyma is more frequent on the extremities, affects both children and elderly people, may be associated with lymphangitis or lymphadenopathy and may heal with scarring.13,14

A

Non-bullous impetigo and bullous impetigo in its crusting stage share a similar appearance on dermoscopy (author’s personal observations). Indeed, both of them are mainly characterized by the presence of diffuse and polygonal crusts resulting from desiccation of exudative fluids, i.e., serum and/ or pus (Figures 9.13B and 9.14A). Cracking of the crusts may give rise to a “dried river bed”-like appearance (Figure 9.14A). Notably, although crusting in dark-skinned patients often features a honey-like hue, in phototypes V and VI it may also display a brownish colour (Figures 9.13B and 9.14A). This is because of the darker colour of the skin shining through the crusts as a result of the normal pigmentation or inflammationinduced brown spots (which may be easily seen in areas not covered by crusts, especially in the healing lesions of bullous impetigo) (Figures 9.13B and 9.14). Interestingly, a white scaling collarette is often visible at the periphery of each crust as well as at the periphery of crusting lesions of bullous impetigo (where it shows an inner free edge) as a result of the previous blister (Figure  9.14B).2 Other less common/less specific features include haemorrhagic areas, patchy dotted vessels (more difficult to see in phototypes V/VI), adherent fabric fibres (clothing threads stuck to the lesion) and white scales (Figures 9.13B and 9.14).2 On the other hand, bullous impetigo in the early stage typically displays non-septate vesicles/blisters with no erythema (differently from eczematous vesicles/bullae that are often septate and associated with erythema and vessels) (Figure  9.15B), whereas ecthyma usually features a thick, round, brown/grey, “oyster shell”-like (concentric) crust resulting from dried serum/pus and necrosis of the epidermis/dermis along with a thick keratotic collarette at the periphery; cracks in the crust may be seen (author’s personal observations) (Figure 9.16B).

B

FIGURE 9.13  Bullous impetigo in the crusting phase in an African boy (A). Dermoscopy: polygonal white/yellow/brown cracked crusts giving rise to a “dried river bed”-like appearance along with haemorrhagic areas, patchy dotted vessels and adherent fabric fibres (B).

118

Bacterial infections A

B

FIGURE 9.14  Dermoscopic magnification of the previous case. “Dried river bed”-like appearance due to cracking of the crusts (A). Peripheral white scales with an inner free edge and central brown structureless pigmentation and fabric fibres (B).

A

B

FIGURE 9.15  Bullous impetigo in the early stages in an African girl (A). Dermoscopy: clear and transparent blister without septae (visible in spongiotic blister) (B).

A

B

FIGURE 9.16  Ecthyma simplex of the back in a South Asian man (A). Dermoscopy: thick, round, brown/grey, “oyster shell”-like (concentric) crust along with a thick keratotic collarette at the periphery; cracks in the crust are also evident (B).

Dermoscopy for skin of colour

119

9.4  Bacterial folliculitis

(Figure 9.17A); the scalp, face, beard and extremities are the most commonly involved sites.13,14 Postinflammatory pigmentation is frequent in darker phototypes.13,14

9.4.1 Introduction Folliculitis is a bacterial infection of the hair follicle more often caused by Staphylococcus aureus.13,14 Mineral oils, plasters and other chemicals clogging the hair follicle orifice may favour such an infection.13,14

9.4.2  Clinical presentation Bacterial folliculitis presents with papules and pustules with centrally placed hairs that may be more or less diffuse

A

9.4.3 Dermoscopy The main dermoscopic feature of bacterial folliculitis is represented by pustules and papules centred by hairs (or patulous ostium) (Figure 9.17B).2 Additionally, a brown network around hairs is often seen as the result of postinflammatory basal layer hyperpigmentation (Figure  9.18A), thereby facilitating retrospective diagnosis and differentiation from macular hyperpigmented dermatoses (authors’ personal observations).

B

FIGURE 9.17  Bacterial folliculitis of the trunk in a Caribbean man with numerous brown macules (A). Dermoscopic examination reveals a pustule centred by a hair (B).

A

B

FIGURE 9.18  Dermoscopy of the lesions from the previous patient: brown reticular areas around the hairs allow the retrospective diagnosis of folliculitis presenting as postinflammatory macules (A). Dermoscopic examination of trichobacteriosis (trichomycosis) axillaris displays waxy and yellowish adherent nodules and concretions localized along the entire length of the hair (B).

120

Bacterial infections

9.5  Corynebacterium-associated dermatoses 9.5.1 Introduction Corynebacteria are small gram-positive cocci generally considered to be commensal organisms, yet they can also be responsible for skin diseases in certain conditions (especially in the case of higher humidity).2,15

9.5.2  Clinical presentation The main dermatoses caused by corynebacteria include trichobacteriosis (trichomycosis) axillaris (adherent granular concretions on axillary hair shafts), pitted keratolysis (crateriform pitting primarily affecting the pressure-bearing aspects of A

the plantar surface of the feet – Figure 9.19A) and erythrasma (asymptomatic, scaly, brownish patches of the folds, especially inguinal and axillary).2,15

9.5.3 Dermoscopy Dermoscopic examination has been showed to be helpful in assisting the diagnosis of both trichobacteriosis (trichomycosis) axillaris and pitted keratolysis.2 In particular, the former condition is typically characterized by waxy and yellowish adherent nodules and concretions localized along the entire length of the hair of the axilla with a global aspect of a flame, skewer or plume (Figure  9.18B), whereas the latter shows a peripheral white-grey/brown-grey scaling collarette having an inner free edge (Figure 9.19B).2 B

FIGURE 9.19  Pitted keratolysis. Clinical image (A). Dermoscopy reveals peripheral white-grey/brown-grey scaling collarette having an inner free edge (B).

REFERENCES

1. Lockwood DNJ. Leprosy. In: Rook’s Textbook of Dermatology (Griffiths CEM, Barker J, Bleiker T, Chalmers R, Creamer D, eds), 9th ed. Oxford: Wiley-Blackwell. 2016:28.1–10. 2. Martín IG, Ankad BS, Errichetti E, Lallas A, Ioannides D, Zaballos P. Bacterial and parasitic infections. In: Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press, 2018:188–209. 3. Kumar B, Dogra S, Kaur I. Epidemiological characteristics of leprosy reactions: 15 years experience from north India. Int J Lepr Other Mycobact Dis 2004;72:125–33. 4. Adhe V, Dongre A, Khopkar U. A  retrospective analysis of histopathology of 64 cases of lepra reactions. Indian J Dermatol 2012;57:114–7. 5. Vinay K, Kamat D, Chatterjee D, Narang T, Dogra S. Dermatoscopy in leprosy and its correlation with clinical spectrum and histopathology: A prospective observational study. J Eur Acad Dermatol Venereol 2019;33:1947–51. 6. Ankad BS, Sakhare PS. Dermoscopy of borderline tuberculoid leprosy. Int J Dermatol 2018;57:74–6. 7. Ankad BA, Sakhare P. Dermoscopy of histoid leprosy: A case report. Dermatol Pract Concept 2017;7:63–5.

8. Charifa A, Mangat R, Oakley AM. Cutaneous tuberculosis. 2020 Sep 1. In: StatPearls [Internet]. Treasure Island, FL: StatPearls Publishing. 2020 Jan. PMID: 29489274. 9. Molpariya A, Ramesh V. Lichen scrofulosorum: Importance of early recognition. Clin Exp Dermatol 2017;42:369–73. 10. Singal A, Bhattacharya SN. Lichen scrofulosorum: A prospective study of 39 patients. Int J Dermatol 2005;44:489‐93. 11. Errichetti E, Ankad BS, Sonthalia S, et  al. Dermoscopy in general dermatology (non-neoplastic dermatoses) in skin of colour: A  comparative retrospective study by the International Dermoscopy Society. Eur J Dermatol 2020. doi: 10.1684/ejd.2020.3928 12. Jassi R, Yadav A, Chander R. Dermoscopy of lichen scrofulosorum. Indian Dermatol Online J 2020;11:876–7. 13. Ayoade KO, Dominguez AR. Bacterial skin infections. In: Dermatology Atlas for Skin of Colour (Jackson-Richards D, Pandya AG, eds), 1st edn. Berlin: Springer-Verlag, 2014:177–87. 14. Tuchman M, Weinberg JM. Bacterial infections. In: Dermatology for Skin of Colour (Kelly AP, Taylor SC, eds), 1st edn. New York: McGraw-Hill Medical, 2009:413–20. 15. DermNet NZ. Corynebacteria. Available at: www. dermnetnz.org/cme/bacterial-infections/corynebacteria (Accessed 1 January 2021)

10 Parasitoses

Parasitoses

Dermoscopy for skin of colour

Enzo Errichetti, Ahmed Sadek, Dalia Hossam, Abhijeet Kumar Jha, Aimilios Lallas and Bengu Nisa Akay

10.1  Cutaneous leishmaniasis 10.1.1 Introduction Leishmaniasis is a protozoal infection transmitted to humans by the bite of infected female sandflies of the genus Phlebotomus (old world – eastern hemisphere), Lutzomyia and Psychodopygus (new world  – Middle and South America).1 Cutaneous leishmaniasis (CL) is mainly caused by Leishmania mexicana and Leishmania braziliensis in the Americas and Leishmania major in all other countries.1,2 Skin lesions caused by L. major usually have a benign course because of mild manifestations and rapid healing, yet some lesions can cause significant disfigurement.1,2

10.1.2  Clinical presentation CL manifests with small red papules that progress over few months to erythematous nodules and plaques with raised borders that may be either scaly/crusted or exudating/ulcerated in the centre (Figures 10.1A–10.3A).3 Lesions may then heal over the course of months but leave depigmented atrophic scars that can cause significant disfigurement in darkskinned patients (Figure 10.4A).3 Satellite lesions and local lymphadenopathy are sometimes present, whereas disseminated CL is reported more uncommonly.4 CL lesions usually affect exposed parts of the body, such as the face, arms and legs, and patients may complain about local pruritus and/or pain.3,4 A

10.1.3 Dermoscopy Dermoscopy of CL in skin of colour is similar to what is usually seen in Caucasian patients, apart from the lower prevalence of vascular structures.5–8 In detail, the most common and characteristic (although not absolutely specific) dermoscopic feature in dark-skinned patients is the presence of white and/or yellow follicular plugs (often referred as “yellow tears”) that histologically correspond to follicular hyperkeratosis (Figures 10.1B and 10.2B).6 Additionally, CL in skin of colour often shows bright white lines due to dermal fibrosis that may be non-specifically distributed or arranged in a radial pattern at the periphery of the lesion, giving rise to a “white starburst” pattern (Figure 10.3B) that is also considered quite characteristic of CL compared with other granulomatous diseases.6 Such a finding is also sometimes visible in scarring lesions (Figure  10.4B), thereby helping the clinician in the retrospective diagnosis. Ulceration/crusting (central or, less commonly, multifocal) and central white scaling are also common but poorly specific.6 Further less frequent findings include structureless bright white areas (especially in long-standing and healing lesions), yellow scales/crusts, vessels (dotted, linear, linearcurved and/or linear with branches  – often surrounded by a white halo and distributed at the periphery of the lesion) and focal orange-yellow structureless areas corresponding to dermal granulomas (“mass effect”) (Figure 10.1B).5–8 Finally, unlike skin lesions, those involving the lips typically do not show follicular plugs but often feature vascular structures surrounded by white halos (authors’ personal observations) (for further details see Section 15.3.5). B

FIGURE 10.1  Cutaneous leishmaniasis of the cheek in an Asian boy (A). Dermoscopic assessment reveals orange structureless areas, focused linear/ linear-branching vessels, bright white lines, patchy white scales and white follicular plugs (B).

DOI: 10.1201/9780367816483-10

122

Parasitoses A

B

FIGURE 10.2  Erysipeloid leishmaniasis in a Bangladeshi man, with a diffuse infiltration of the right cheek and nose without ulceration (A). Dermoscopy shows several follicular keratotic plugs (B).

A

B

FIGURE 10.3  Cutaneous leishmaniasis of the dorsum of the feet in a North African man (A). Dermoscopy: central erosion covered by a yellow crust along with a peripheral white halo displaying radial linear projections (arrows) (“white starburst” pattern) (B).

A

B

FIGURE 10.4  Cutaneous leishmaniasis of the dorsum of the leg in a North African man (A). Dermoscopy: ulcerations with yellow crusts, bright white structureless areas and peripheral white projections (arrows); linear and dotted vessels (arrowhead) are also evident at the periphery (B).

123

Dermoscopy for skin of colour

10.2 Demodicosis 10.2.1 Introduction Demodicosis is a cutaneous infestation due to human Demodex mites (Demodex folliculorum and Demodex brevis) involving the pilosebaceous unit. It is typically classified into a primary form and a secondary form (associated with systemic or local immunosuppression).5

Additionally, it is possible to see non-protruding white follicular plugs (corresponding to a less dense mixture of mites and keratin) (Figure 10.5B) and several other unspecific dermoscopic features, whose prevalence varies according to the subtypes of demodicosis, including erythema, scaling, pustules and reticular dilated vessels.5,9,10

10.3 Scabies

10.2.2  Clinical presentation

10.3.1 Introduction

Several clinical variants of primary demodicosis have been recognized, including pityriasis folliculorum, papulopustular demodicosis (Figure  10.5A), periorificial demodicosis (perioral, periocular and/or periauricular), ocular demodicosis and nodulocystic demodicosis.5,9 The face (especially the periorificial areas) is the typical involved area; lesions are often asymmetric and grouped in irregular configurations with satellite lesions.5,9 On the other hand, secondary forms have a more diffuse distribution, with widespread facial lesions and/or trunk involvement.5,9

Scabies is a skin infestation caused by the mite Sarcoptes scabiei var. hominis, which is transmitted by close contacts or, less commonly, via fomites (e.g., clothing and bed sheets). A classic form of scabies is typified by around 10 to 20 mites on the entire body, yet the mite’s number is far higher (thousands) in crusted scabies (mainly seen in immunocompromized patients).5

10.2.3 Dermoscopy Dermoscopy in demodicosis in dark-skinned patients may be particularly helpful to differentiate such a condition from clinically similar dermatoses. In detail, the most peculiar dermoscopic finding is represented by protruding white follicular plugs (previously known as “Demodex tails”) (Figure 10.5B) that represent a mixture of keratin and aggregates of mites under magnification.5,6,9,10 Notably, they need to be distinguished from “sebum excrescences” (protruding/ non-protruding follicular plugs corresponding to sebum and keratin deposits in follicles) visible in facial seborrheic dermatitis in dark-skinned patients, which are usually broader and shorter than the protruding follicular plugs seen in demodicosis.6

A

10.3.2  Clinical presentation Scabies is typified by an intense nocturnal pruritus along with burrows (short serpiginous lines) as well as non-specific lesions (e.g., erythematous papules, vesicles and excoriations) involving typical areas, such as the interdigital spaces, volar surface of the wrist, axillae, nipples, external genitalia and buttocks (Figure 10.6A).5 Nodules may also be observed, especially in the genital areas (Figure 10.7A). On the other hand, crusted scabies manifests as diffuse scaly/crusted erythematous plaques.5

10.3.3 Dermoscopy Dermoscopic assessment may be of significant aid in ­detecting the mite and guiding the skin scraping for microscopic ­analysis.5,11 In detail, mites appear as single or ­multiple (especially in crusted scabies) dark brown, ­triangular structures located at the end of whitish-greyish wavy lines (“delta-wing jets with contrail” sign) (Figures  10.6B and 10.7B).5,11 The

B

FIGURE 10.5  Demodicosis in an African woman (A). Dermoscopy reveals the typical protruding white follicular plugs (previously known as “Demodex tails”) that represent a mixture of keratin and aggregates of mites under magnification (B).

124 t­ riangular structures correspond to the pigmented anterior part of the mite (mouth and two anterior pairs of legs), whereas the wavy lines represent the mite burrows with eggs and faecal pellets (scybala) inside.5 Notably, eggs may be seen on high magnification videodermoscopy.5

A

Parasitoses Besides diagnostic purpose, high magnification videodermoscopy may be of aid in monitoring treatment efficacy as it may show the absence of mite migration and progressive degradation of the mite with replacement with an amorphous material after an effective therapy.5

B

FIGURE 10.6  Scabies in a South Asian boy presenting as small papules of the dorsal aspect of the forearms and hands (A). Dermoscopy: dark brown triangular structure (representing the anterior part of the mite) located at the end of a whitish-greyish wavy line (burrow) (“delta-wing jets with contrail” sign) (magnification in the inset) (B).

A

B

FIGURE 10.7  Nodular scabies of the penis in an African man (A). Dermoscopy shows the so-called “delta-wing jets with contrail” sign (magnification in the inset) (B).

125

Dermoscopy for skin of colour

excoriations, lichenification, hyperchromic lesions and haemorrhagic lesions mainly located on the trunk, abdomen and buttocks.5

10.4 Pediculosis 10.4.1 Introduction Pediculosis is an infestation due to human lice which spreads from person to person by close contact and, less commonly, via fomites.5 Different species prefer to feed in specific locations on the host, with body lice (Pediculus humanus corporis) infesting clothing and laying their eggs (“nits”) on fibres in the fabric seams and head (Pediculus humanus capitis) and pubic lice (Phthirus pubis) affecting the hair and laying their eggs at the base of hair shafts.5

10.4.2  Clinical presentation Both pediculosis capitis and pediculosis pubis present with intense pruritus, excoriations, erythema and scaling, with the former affecting the scalp and posterior neck and the latter involving the pubic area (albeit the trunk, limbs and eyelashes hairs may also be affected in heavy infestations).5 Notably, blue-grey macules (maculae ceruleae) may also be found in pediculosis pubis.5 On the other hand, in pediculosis corporis, pruritus is associated with pinpoint red macules, urticarial papules,

A

10.4.3 Dermoscopy Dermoscopic examination assists the clinician in identifying both the adult lice and/or viable nits fixed to the hair shaft.5 In particular, head and body lice are 2–4  mm in size and feature an elongated dark grey-brown body, three pairs of clawed legs and narrow anterior mouthparts (Figure 10.8A), whereas pubic lice reveal the typical grey, short, broad body (with rather stout claws on the middle and hind legs) and large middle and hind legs, which have thick claws for grasping hairs (Figure 10.8B).5 When it comes to nits, three different morphological types exist, including viable nits (ovoid brown structures with operculum) (Figure  10.9A), abortive nits (containing n­on-viable embryo and air spaces) (Figure 10.9B) and empty nits (translucent involucrum with a plane free ending devoid of operculum) (Figure 10.9C).5 Of note, both lice and viable nits are sometimes difficult to see in skin of colour because of the dark shade of the background (hairs and skin).5

B

FIGURE 10.8  Dermoscopic view of adult head louse with a 3–4 mm long, dark greyish-brown dorso-ventrally flattened body, one pair of antennae and three pairs of legs (A). Dermoscopy of pubic louse reveals a broad body, large middle and hind legs, bearing thick claws grasping the pubic hairs (B). (Adapted from Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press.)

A

B

C

FIGURE 10.9  Dermoscopy images of nits. Pediculosis capitis (viable nit): dark brown-coloured closed viable nit with tense convex walls and an intact operculum (white arrow) containing viable embryo (A). Pediculosis capitis (abortive nit): some air spaces (white arrow) with condensed non-viable embryo (white arrowhead) (B). Pediculosis capitis (empty nit): translucent whitish open empty nit without the operculum, representing empty cases after the discharge of the nymph or abortive embryo (C). (Adapted from Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press.)

126

Parasitoses crusts (Figure 10.10A).5 The larva usually enters the skin and after about 4 days begins to burrow within the epidermis at a rate of 1 to 2 cm per day. Systemic involvement is quite rare (Loeffler syndrome).5

10.5  Cutaneous larva migrans 10.5.1 Introduction Cutaneous larva migrans, also known as creeping eruption, is a skin infestation due to the larvae of hookworms (helminths) infecting domestic dogs and cats (Ancylostoma braziliense, Ancylostoma caninum and Uncinaria stenocephala).5 It is more common in warm tropical climates and acquired by direct contact with either contaminated soil/sand or dog/cat faeces containing the larvae.5

10.5.2  Clinical presentation

10.5.3 Dermoscopy Handheld (×10 magnification) dermoscopic examination may show translucent brownish structureless areas in a serpiginous segmental arrangement when the larva is present (Figure 10.10B), whereas dotted vessels may be appreciated in areas where the burrow is empty.5 Notably, low magnification is not enough to directly highlight the larvae.5

It typically manifests as very itchy, serpiginous/curvilinear, more or less erythematous tracts, with or without vesicles and A

B

FIGURE 10.10  Cutaneous larva migrans in an African woman (A). Dermoscopy displays translucent brownish structureless areas in a serpiginoussegmental arrangement where the larva is located (B). (From Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press.)

REFERENCES 1. Maurer M, Dondji B, von Stebut E. What determines the success or failure of intracellular cutaneous parasites? Lessons learned from leishmaniasis. Med Microbiol Immunol 2009;198:137–46. 2. David CV, Craft N. Cutaneous and mucocutaneous leishmaniasis. Dermatol Ther 2009;22:491–502. 3. Magill AJ. Cutaneous leishmaniasis in the returning traveler. Infect Dis Clin North Am 2005;19:241–66. 4. Sinha PK, Pandey K, Bhattacharya SK. Diagnosis & management of leishmania/HIV co-infection. Indian J Med Res 2005;121:407–14. 5. Martín IG, Ankad BS, Errichetti E, Lallas A, Ioannides D, Zaballos P. Bacterial and parasitic infections. In: Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press, 2018:188–209. 6. Errichetti E, Ankad BS, Sonthalia S, et al. Dermoscopy in general dermatology (non-neoplastic dermatoses) in

skin of colour: A comparative retrospective study by the I­nternational Dermoscopy Society. Eur J Dermatol 2020. doi: 10.1684/ejd.2020.3928 7. Llambrich A, Zaballos P, Terrasa F, Torne I, Puig S, Malvehy J. Dermoscopy of cutaneous leishmaniasis. Br J Dermatol 2009;160:756–61. 8. Yücel A, Günas¸ti S, Denli Y, Uzun S. Cutaneous leishmaniasis: New dermoscopic findings. Int J Dermatol 2013;52:831–7. 9. Segal R, Mimouni D, Feuerman H, Pagovitz O, David M. Dermoscopy as a diagnostic tool in demodicidosis. Int J Dermatol 2010;49:1018–23. 10. Errichetti E. Dermoscopy of inflammatory dermatoses (Inflammoscopy): An up-to-date overview. Dermatol Pract Concept 2019;9:169–80. 11. Errichetti E, Stinco G. Dermoscopy in general dermatology: A  practical overview. Dermatol Ther (Heidelb) 2016;6:471–507.

11 Mycoses

Mycoses

Dermoscopy for skin of colour

Enzo Errichetti, Balachandra Ankad, Manas Chatterjee, Piergiacomo Calzavara Pinton, Vincenzo Maione and Payal Chauhan

11.1  Tinea corporis 11.1.1 Introduction Tinea corporis is a superficial fungal infection involving glabrous skin (i.e., trunk and limbs, excluding specialized sites such as the scalp [tinea capitis], feet [tinea pedis], palmar areas [tinea manuum] and groin [tinea cruris]) that is caused by the invasion and proliferation of dermatophytes in the stratum corneum.1 Three modes of transmission are reported, including human to human, animal to human and soil to human transmission.1

11.1.2  Clinical presentation Tinea corporis classically manifests as asymptomatic or itchy, single or few, erythematous, circular, or annular scaly plaques that often display central clearing giving rise to an expanding ring-like lesion and a well-demarcated margin that may be papular, pustular, or vesicular (Figures 11.1A–11.3A).1 In very dark phototypes, lesions are commonly less erythematous and more pigmented (Figure 11.1A).1 The term trichophytic Majocchi granuloma refers to a deep follicular involvement with perifollicular granulomatous/ fibrotic reaction that manifests as a solitary or multiple persistent papulopustules or crusted plaques (Figure 11.4A).1

A

11.1.3 Dermoscopy The main dermoscopic feature of tinea corporis in skin of colour is represented by a peripheral white scaling collarette that characteristically shows a jagged outer free edge (Figures 11.1B–11.3B), yet a mixed free edge (both inner and outer) may also sometimes be seen (Figure 11.3B).2,3 This particular scaling pattern results from the peculiar centrifugal peeling direction of tinea corporis, thereby letting the clinician differentiate such a condition from other annular papulosquamous dermatoses (e.g., pityriasis rosea and annular psoriasis) that generally present an inner free edge.2,3 Moreover, broken/ absent hairs in the centre of the lesions (Figure 11.1B) as well as peripheral yellow and brown scales (Figure 11.2B) may also be commonly found in tinea corporis, but they are not absolutely specific.2 Additionally, peripheral vessels (mainly dotted), pigmentary structures, including brown dots or focal/diffuse brown structureless areas, and fabric fibres may also be observed in tinea corporis affecting dark-skinned patients.2,3 Finally, trichophytic Majocchi granuloma is typified by pustules, crusting, broken/absent hairs and perifollicular yellow-white areas (corresponding to perifollicular granulomas/ fibrosis) (Figure 11.4B) (authors’ personal observations).

B

FIGURE 11.1  Tinea corporis in an African man (A). Dermoscopy reveals a peripheral white scaling collarette having a jagged mixed free edge (both inner and outer); broken hairs are also evident (B).

DOI: 10.1201/9780367816483-11

128

Mycoses A

B

FIGURE 11.2  Tinea corporis of the dorsum of the right hand in an Indian man (A). Dermoscopic examination shows peripheral scaling with both inner and outer free margins; peripheral brown dots and pustules are also present (B).

A

B

FIGURE 11.3  Tinea corporis of the chest in an Indian woman (A). Dermoscopy: peripheral scaling with both inner and outer free borders (B).

A

B

FIGURE 11.4  Trichophytic Majocchi granuloma of the forearm in an Indian man (A). Dermoscopy: pustules, crusting, broken/absent hairs and perifollicular yellow-white areas (B).

129

Dermoscopy for skin of colour

11.2  Tinea capitis 11.2.1 Introduction Tinea capitis is the most common paediatric dermatophyte infection worldwide, with a particular predilection for black populations (Afro-Caribbean and African American children).4,5 Its incidence is highest in 3- to 7-year-old children, and Microsporum and Trichophyton groups represent the main fungal agents causing tinea capitis.4,5

11.2.2  Clinical presentation Several clinical presentations of tinea capitis do exist in darkskinned patients, including less inflammatory and inflammatory forms.4,5 Multifocal loss of hair with black dots (Figure 11.5A), diffuse white scaling, single or multiple scaling grey patches (Figure 11.6A) and moth eaten-like alopecia are part of the former group, whereas kerion celsi is the most serious inflammatory variant, with alopecic plaques associated with pustules and crusts that may lead to scarring and permanent alopecia (Figure 11.7A).4,5 A

11.2.3 Dermoscopy Several peculiar dermoscopic findings related to fungal invasion of the hair shaft may be seen in tinea capitis, including “comma” hairs, “Morse-code” hairs, “zig-zag” hairs, broken hairs and black dots, with the first two being the most common/characteristic ones (Figures 11.5B and 11.7B).6–10 In detail, “comma” hairs are short, broken and bent hair shafts showing a C-shaped appearance, whereas “Morsecode” hairs (also called interrupted hairs) are typified by hair shafts displaying alternating whitish and brown bands.6–10 Notably, in African people and subjects with curly hairs, “comma” hairs often show a “corkscrew” aspect (Figure 11.5B).6–10 Importantly, white scaling, often enveloping the hairs, may sometimes be the main dermoscopic feature of non-inflammatory forms in skin of colour (Figure  11.6B).6–10 Similarly, dermoscopic examination often reveals only non-specific features in kerion celsi, including erythema, scaling, pustules and crusts, yet some of the aforementioned typical findings may also be found (Figure 11.7B).6–10

B

FIGURE 11.5  Tinea capitis (multifocal loss of hair with black dots) in an African infant (A). Dermoscopic assessment shows loss of hair along with comma-like and corkscrew-like hairs (B).

A

B

FIGURE 11.6  Tinea capitis (multiple white scaling patches with hair loss) in an African boy (A). Dermoscopy displays white scaling enveloping the hairs and loss of hair (B).

130

Mycoses A

B

FIGURE 11.7  Kerion celsi in an African boy. Clinical appearance (A). Dermoscopic examination shows unspecific findings (i.e., crusts and pustules) as well as black dots and “Morse-code” hairs (better visible in the boxed area) (B). (From Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press.)

11.3  Pityriasis versicolour 11.3.1 Introduction Pityriasis versicolour is a superficial fungal infection due to Malassezia furfur, which is part of the normal skin flora (under the yeast phase – Pityrosporum orbiculare) and grows into the hyphal phase (Malassezia furfur), which is responsible for the clinical manifestations.1

11.3.2  Clinical presentation Pityriasis versicolour in skin of colour usually presents as round or oval macules coalescing into larger patches that most commonly involve the upper chest/back (Figures  11.8A–11.11A) and, less commonly, the arms and face.1 The colour of the lesions may be white (hypopigmented forms) or dark brown (hyperpigmented forms), whereas the skin surface usually

A

displays a fine white scaling (Figures 11.8A–11.11A).1 Notably, in dark-skinned patients, it is not uncommon to see thicker pigmented plaques (Figure 11.8A).1

11.3.3 Dermoscopy The most specific dermoscopic features of pityriasis versicolour, both hypo- and hyperpigmented variants, include white scaling distributed in the skin furrows (Figures  11.8B and 11.9B) and perifollicular white scales (Figure  11.10B) that are related to the tropism for more humid/greasy areas (skin furrows and follicles).2 Additionally, perifollicular hypopigmentation (Figure 11.11B) is considered another peculiar dermoscopic finding in both hypo- and hyperpigmented lesions and is also seen in non-active cases, thereby facilitating the retrospective diagnosis.2 Further non-specific findings include brown reticular or structureless areas (brown lesions) and white background (white lesions).2

B

FIGURE 11.8  Hyperpigmented pityriasis versicolour in an Indian man (A). Dermoscopy reveals a brown structureless background along with white scales in the furrows and perifollicular white hypopigmentation (B).

131

Dermoscopy for skin of colour A

B

FIGURE 11.9  Hypopigmented pityriasis versicolour in an Indian woman (A). Dermoscopy: white scales in the furrows over an ill-defined white background (B).

A

B

FIGURE 11.10  Sparse brown patches in a case of pityriasis versicolour in an Indian man (A). Dermoscopy: brown reticular network along with perifollicular white hypopigmentation (B).

A

B

FIGURE 11.11  Hyperpigmented pityriasis versicolour in an Indian man (A). Dermoscopy: perifollicular white scaling (B).

132

Mycoses A

B

FIGURE 11.12  Tinea nigra in a Hispanic boy. Clinical appearance (A). Dermoscopy reveals the typical pattern consisting of superficial fine, wispy, light brown strands that form a reticular-like patch having a uniform brown colour (B). (From Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press.)

11.4  Tinea nigra 11.4.1 Introduction Tinea nigra is a superficial fungal infection mainly involving palms and soles related to Hortaea werneckii, a yeast-like hyphomycete, more typical of hot tropical areas.11,12

11.4.2  Clinical presentation Tinea nigra is clinically typified by a single or multiple (more uncommonly) brown or black patches on the palms and/or soles (Figure 11.12A).11,12 Because of its clinical presentation, it is often mistaken for melanocytic lesions.11,12

11.4.3 Dermoscopy Dermoscopic assessment typically reveals an overall reticulated pattern, composed of peculiar pigmented spicules that do not follow furrows and ridges, unlike melanocytic lesions (Figure 11.12B).12,13 More uncommon patterns include brownish bundles of spicules or dotted/granule-like structures arranged in a parallel ridge pattern.12,13

11.5  Mycetoma (Madura foot) 11.5.1 Introduction Mycetoma, also known as Madura foot, is a soft tissue infection associated with a chronic suppurative or granulomatous reaction due to the inoculation of a fungus (eumycetoma) or an actinomycete (actinomycetoma) often following a traumatic abrasion of the skin.14,15 The disease is endemic in tropical areas, such as sub-Saharan Africa, Asia or South America.14,15

11.5.2  Clinical presentation It classically manifests as soft tissue swelling along with sinus tracts that sometimes drain macroscopic grains (representing microbic agglomeration) whose colour varies according to the etiological agent, with white-yellow and red grains being more commonly associated with actinomycetes (Figure 11.13A) and white and dark/black grains usually related to fungal infections.14,15 The lower extremities and plantar areas are the most commonly involved areas, with possible consequent functional difficulties in walking.14,15 The course of the disease is extremely slow and spontaneous regression is quite rare.14,15 In general, eumycetoma is paucisymptomatic and deep involvement tends to be less common, whereas actinomycetoma does have an osteolytic potential and can be associated with systemic symptoms, including weight loss, anaemia and fever.14,15

11.5.3 Dermoscopy Dermoscopy of mycetoma in dark-skinned patients is characterized by multiple papules disrupting the physiological dermatoglyphics/skin furrows and displaying fistulous tracts extruding grains displaying a different colour depending on the causal agent (see Clinical presentation) (Figure  11.13B);16,17 reduction or disappearance of fingerprints/skin furrows may also be seen in areas with no apparent papule because of epidermal-dermal junction flattening resulting from the inflammatory infiltrate (Figure 11.13B).16,17 Additional less specific dermocopic findings include blood spots, erosions, orange-yellowish structureless areas (corresponding to the granulomatous infiltrate) and brown structureless areas (Figure 11.13B).16,17

133

Dermoscopy for skin of colour A

B

FIGURE 11.13  Actinomycetoma of the foot in an African female (A). Dermoscopic examination shows a papule (arrow) disrupting the physiological dermatoglyphics and displaying a fistulous tract extruding white-yellowish grains; multiple focal brown structureless areas with reduction of skin furrows and blood spots are also evident (B).

A

B

FIGURE 11.14  Fixed cutaneous sporotrichosis in an Indian female. Clinical appearance (A). Dermoscopy reveals diffuse background erythema, yellowish-orange areas and yellow follicular keratotic plugs; vessels and white scales are also appreciated (B).

11.6 Sporotrichosis 11.6.1 Introduction Sporotrichosis is a mycotic infection involving the skin and subcutaneous tissue following traumatic inoculation caused by a saprophytic organism, Sporothrix schenckii.18

11.6.2  Clinical presentation Sporotrichosis usually presents as a gradually enlarging papulo-nodule at the site of the trauma, which may remain as such (fixed cutaneous sporotrichosis) (Figure 11.14A) or evolve into multiple nodules along lymphatics (lymphocutaneous sporotrichosis); ulceration may be present.18

11.6.3 Dermoscopy Dermoscopic assessment reveals diffuse erythema and yellowish-orange areas in an evolving lesion with white fibrotic strands present in late lesions; vessels, ulceration, crusting and follicular keratotic plugs can also be visualized (Figure 11.14B).19,20

11.7 Chromoblastomycosis 11.7.1 Introduction Chromoblastomycosis is a subcutaneous mycosis caused by traumatic inoculation of a dematiaceous group of fungi, such as Fonsecaea pedrosoi, Phialophora verrucosa and Cladophialophora carrionii.21

134

Mycoses

11.7.2  Clinical presentation

11.7.3 Dermoscopy

Lesions of chromoblastomycosis may initially start as papules located over exposed sites that can gradually evolve into a polymorphic clinical presentation, including nodular, tumoral, verrucous, cicatricial and plaque-type lesions (Figure 11.15A).21

Dermoscopic examination mainly reveals yellowish-orange areas, pink and white areas and reddish-brown dots; scales, crusts and polymorphic vessels can also be seen. (Figure 11.15B).20,22 The yellowish-orange areas correspond to underlying granuloma with reddish-brown dots representing transepidermal elimination of fungal elements, inflammatory cells and hemorrhage.20,22

A

B

FIGURE 11.15  Chromoblastomycosis in an Indian female. Clinical appearance (A). Dermoscopy displays multiple reddish-brown dots, yellowishorange areas, pink and white areas with vessels and yellow and white scales (B).

REFERENCES 1. Jackson-Richards D. Tinea corporis, tinea versicolour, and candidiasis. In: Dermatology Atlas for Skin of Colour (Jackson-Richards D, Pandya AG, eds), 1st edn. Berlin: Springer-Verlag, 2014:189–94. 2. Errichetti E, Ankad BS, Sonthalia S, et  al. Dermoscopy in general dermatology (non-neoplastic dermatoses) in skin of colour: A  comparative retrospective study by the International Dermoscopy Society. Eur J Dermatol 2020. doi: 10.1684/ejd.2020.3928 3. Ankad BS, Mukherjee SS, Nikam BP, Reshme AS, Sakhare PS, Mural PH. Dermoscopic characterization of dermatophytosis: A  preliminary observation. Indian Dermatol Online J 2020;11:202–7. 4. Nakamura M, Gathers RC. Tinea capitis. In: Dermatology Atlas for Skin of Colour (Jackson-Richards D, Pandya AG, eds), 1st edn. Berlin: Springer-Verlag, 2014:195–200. 5. Dogo J, Afegbua SL, Dung EC. Prevalence of tinea capitis among school children in nok community of Kaduna State, Nigeria. J Pathogens 2016;2016:9601717. 6. Rudnicka L, Szepietowski JC, Slowinska M, Lukomska M, Maj M, Pinheiro AM. Tinea capitis. In: Atlas of Trichoscopy: Dermoscopy in Hair and Scalp Disease (Rudnicka L, Olszewska M, Rakowska A, eds), 1st edn. London: Springer-Verlag, 2012:361–9. 7. Olarinoye GM, Katibi OS, Ilesanmi ON, Fayemiwo SA, Ogunbiyi AO, George AO. Trichoscopic features of tinea















capitis among primary school children in north central Nigeria. Int J Dermatol 2020;59:1346–52. 8. Brasileiro A, Campos S, Cabete J, et al. Trichoscopy as an additional tool for the differential diagnosis of tinea capitis. Br J Dermatol 2016;175:208–9. 9. Kumar P, Pandhi D, Bhattacharya SN, Das S. Trichoscopy as a diagnostic tool for tinea capitis: A prospective, observational study. Int J Trichol 2020;12:68. 10. Isa RI, Amaya BY, Pimentel MI, et al. Dermoscopy in tinea capitis: A prospective study on 43 patients. Med Cutan Iber Lat Am 2014;42:18–22. 11. Bonifaz A, Gómez-Daza F, Paredes V, Ponce RM. Tinea versicolour, tinea nigra, White Piedra, and Black Piedra. Clin Dermatol 2010;28:140–5. 12. Veasey JV, Avila RB, Miguel BAF, Muramatu LH. White Piedra, Black Piedra, tinea versicolour, and tinea nigra: Contribution to the diagnosis of superficial mycosis. An Bras Dermatol 2017;92:413–6. 13. Nazzaro G, Ponziani A, Cavicchini S. Tinea nigra: A diagnostic pitfall. J Am Acad Dermatol 2016;75:e219–e20. 14. Wang SSY. Madura foot in a developed tropical country. Int J Infect Dis 2020;101:312–3. 15. Emery D, Denning DW. The global distribution of actinomycetoma and eumycetoma. PLoS Negl Trop Dis 2020;14:e0008397. 16. Litaiem N, Midassi O, Zeglaoui F. Detecting subclinical mycetoma’s black grains using dermoscopy. Int J Dermatol 2019;58:231–2.

Dermoscopy for skin of colour 17. Reis LM, Lima BZ, Zillo Fda C, Rezende CM, Fabricio LH, Pinto CA. Dermoscopy assisting the diagnosis of mycetoma: Case report and literature review. An Bras Dermatol 2014;8:832–3. 18. Mahajan VK. Sporotrichosis: An overview and therapeutic options. Dermatol Res Pract 2014;272376. 19. Vinay K, Bhattacharjee R, Bishnoi A, Chatterjee D, Rudramurthy S, Dogra S. Dermatoscopic features of cutaneous sporotrichosis. J Eur Acad Dermatol Venereol 2020;34:e718–e20.

135 20. Chauhan P, Adya KA. Dermatoscopy of cutaneous granulomatous disorders. Indian Dermatol Online J 2021;12:34–44. 21. Queiroz-Telles F, Esterre P, Perez-Blanco M, Vitale RG, Salgado CG, Bonifaz A. Chromoblastomycosis: An overview of clinical manifestations, diagnosis and treatment. Med Mycol 2009;47:3–15. 22. Chauhan P, Jindal R, Shirazi N. Dermoscopy of chromoblastomycosis. Indian Dermatol Online J 2019;10:759–60.

12 Viral infections

Viral infections

Dermoscopy for skin of colour

Feroze Kaliyadan, Jayasree Puravoor, Ahmed Sadek, Dalia Hossam and Enzo Errichetti

12.1  Common, plane and genital warts 12.1.1 Introduction Viral infections are quite common in dark skin, especially in the paediatric population and young adults, with human papillomavirus (HPV)-related warts being the most frequent ones. They typically spread through direct skin-to-skin contact and less commonly via fomites (e.g., towels).1 Several clinical variants of warts because of different HPV genotypes do exist, mainly including common warts (verrucae vulgaris) (HPV 1, 2 and 4), plane warts (HPV 3, 10, 26–29 and 41) and genital warts (condylomata acuminata) (HPV 6 and 11).1

12.1.2  Clinical presentation Common warts appear as exophytic, verrucous, domeshaped papules or plaques of variable size (usually 1 to 10  mm) that may display multiple black dots (thrombosed capillaries) over the surface (Figures  12.1A and 12.2A).1 They more c­ommonly involve the hands (especially the fingers), although they may occur anywhere.1 In the plantar regions, warts are generally endophytic, painful at pressure and may sometimes coalesce into a cobblestone pattern (mosaic warts).1 Plane warts present as multiple, flat-topped, smooth, skin-coloured or brownish papules most frequently affecting the face and the dorsal aspects of the hands and arms (Figure  12.3A), whereas condylomata acuminata typically consist of exophytic, sessile or pedunculated, soft, pinkish or brownish papules of variable sizes of the anogenital skin and/ or mucous membranes (Figure  12.4A), which may become confluent as cauliflower-like plaques.1

12.1.3 Dermoscopy Dermoscopic features of common warts vary according to the localization. In particular, lesions localized on the volar skin of the hands and feet may show dermatoglyphics interruption, vessels (more commonly dotted and linear with a white halo), finger-like projections containing elongated/dilated vessels surrounded by whitish halos (exophytic lesions) and purpleblack dots and linear/structureless areas (representing thrombosed vessels and intraepidermal haemorrhages, respectively); a brownish background is also typically seen in darker phototypes (Figure 12.1B).2–4 On the other hand, lesions of non-palmoplantar areas usually display only black dots corresponding to small thrombosed vessels over a brownish or bluish (in very dark skin) background (Figure  12.2B).2 A  bluish hue might result from an optical effect due to the presence of acanthosis on a high overlying melanin density.2 White lines may also be found on polarized-light dermoscopy (Figure 12.2B).2–4 Plane warts typically feature homogeneous white areas having roundish or irregular borders (Figure  12.3).2–4 Although diffuse dotted vessels may be seen in the context of white areas, in dark-skinned patients it is not uncommon to see only brownish dots (Figure 12.3B).2 Genital warts may show different dermoscopic patterns.3,4 In detail, sessile/flat lesions display a whitish network circumscribing areas centred by dilated dotted or glomerular vessels (mosaic pattern), whereas pedunculated lesions feature irregular whitish projections, corresponding to papillomatosis, hyperkeratosis and acanthosis, comprising elongated and dilated vessels (finger-like pattern) (Figure  12.4B).2–4 Like common warts, in very dark-skinned patients, vessels may be difficult to see and the background may be bluish (Figure  12.4B).2 Importantly, dermoscopy may help differentiate genital warts from clinically similar conditions, e.g., penile Fordyce spots (Figure 12.5) and acquired lymphangiectasia (Figure 12.6).

DOI: 10.1201/9780367816483-12

138 A

Viral infections B

FIGURE 12.1  Common viral warts of the second left finger in an African woman (A). Dermatoglyphics interruption as well as dotted vessels and haemorrhagic spots over a brownish mosaic-like background are evident on dermoscopy (B).

A

B

FIGURE 12.2  Common viral warts of the lower arm in an African boy (A). Dermoscopy displays black dots and white lines over a bluish background (B).

A

B

FIGURE 12.3  Plane warts of the forehead in an Indian girl (A). Dermoscopic examination shows homogeneous white areas having irregular borders and brownish dots (better seen in the inset) (B).

139

Dermoscopy for skin of colour A

B

FIGURE 12.4  Pedunculated genital warts (clinical image) (A). Dermoscopy displays irregular bluish-whitish projections having a common base (finger-like pattern) (B).

A

B

FIGURE 12.5  Penile Fordyce spots in an African man (A). Dermoscopic assessment reveals yellowish globules (B).

A

B

FIGURE 12.6  Acquired lymphangiectasia in an African woman (A). Dermoscopic assessment shows orangish-yellowish lacunae separated by white septae; some haemorrhagic spots are also present (B).

140

Viral infections lesions are mainly located on the face, neck and chest, whereas the genital and perigenital areas are more commonly involved in adults.4,5

12.2  Molluscum contagiosum 12.2.1 Introduction Molluscum contagiosum is a common skin infection in skin of colour that is due to a DNA poxvirus (Molluscipox virus) and may spread through direct contact or vehicles.4,5 It is more frequently seen in children and young adults (in whom it represents a sexually transmitted disease).4,5

12.2.2  Clinical presentation The typical lesions of molluscum contagiosum are single or multiple, umbilicated, smooth, skin-coloured papules (Figures  12.7A and 12.8A).4,5 Even though they are usually asymptomatic, they may sometimes cause pruritis, especially in the case of inflammation.4,5 In the paediatric population, the A

12.2.3 Dermoscopy The main dermoscopic feature of molluscum contagiosum in skin of colour is represented by globular white areas (histologically corresponding to the well-defined, lobulated, endophytic epidermal hyperplasia characteristic of this viral infection), which may be single or multiple forming either polylobular structures or four-leaf clover-like aspect (Figure 12.7B).2,4 Of note, globules may appear as white rosettes on polarized-light dermoscopy (Figure  12.7B).2,4 A  central orifice/depression may also be seen (Figure  12.8B), whereas, differently from Caucasian patients, peripheral vessels (dotted or crown-like) are difficult to see.2,4 B

FIGURE 12.7  Molluscum contagiosum of the perioral area in an African girl (A). Dermoscopy: bright white globules which appear as white rosettes on polarized light (inset) (B).

A

B

FIGURE 12.8  Molluscum contagiosum of the trunk in a Caribbean boy (A). Dermoscopic examination displays a central white globule (B).

141

Dermoscopy for skin of colour

12.3  Hand, foot and mouth disease 12.3.1 Introduction Hand, foot and mouth disease (HFMD) is a viral exanthem caused by human enteroviruses and coxsackieviruses most commonly occurring in children under 10 years of age, which is characterized by a low-grade fever followed by a skin and mucosal rash.6

12.3.2  Clinical presentation Cutaneous presentation of HFMD typically consist of asymptomatic or tender lesions varying from erythematous papules to oval-shaped vesicles favouring the palms and soles

A

(Figure 12.9A), although the buttocks, knees and elbows may also sometimes be involved.6 Oral ulcers can be seen and, if present, are usually painful.6

12.3.3 Dermoscopy Dermoscopic examination of vesicles of HFMD usually displays a yellowish area surrounded by a rim of erythema; white dots corresponding to eccrine sweat glands openings are usually seen on palmo-plantar areas (Figure 12.9B) (authors’ personal observations). Such a dermoscopic pattern is different from those of other common conditions that may involve the hands and feet, including herpes simplex infections and pompholyx respectively showing orangish vesicles with a yellow centre and orangish vesicles separated by white septae (Figure 12.10).

B

FIGURE 12.9  Hand, foot and mouth disease (hand blister) in a Middle Eastern boy (A). Dermoscopy shows a yellowish area surrounded by a rim of erythema; white dots corresponding to eccrine sweat glands openings are also evident (B).

A

B

FIGURE 12.10  Dermoscopy of herpes simplex infections (A) and pompholyx (B) respectively displays orangish vesicles with a yellow centre and orangish vesicles separated by white septae.

142

REFERENCES

1. Strickland A, Blanco G. Human papillomavirus (HPV). In: Dermatology Atlas for Skin of Colour (Jackson-Richards D, Pandya AG, eds), 1st edn. Berlin: Springer-Verlag, 2014:201–7. 2. Errichetti E, Ankad BS, Sonthalia S, et  al. Dermoscopy in general dermatology (non-neoplastic dermatoses) in skin of colour: A  comparative retrospective study by the International Dermoscopy Society. Eur J Dermatol 2020. doi: 10.1684/ejd.2020.3928

Viral infections 3. Piccolo V. Update on dermoscopy and infectious skin diseases. Dermatol Pract Concept 2019;10:e2020003. 4. Lacarrubba F, Verzì AE, Micali G. Viral infections. In: Dermoscopy in General Dermatology (Lallas A, Errichetti E, Ioannides D, eds), 1st edn. Boca Raton, FL: CRC Press, 2018:221–7. 5. Silverberg NB. Pediatric molluscum: An update. Cutis 2019;104:301–5. 6. Saguil A, Kane SF, Lauters R, Mercado MG. Hand-footand-mouth disease: Rapid evidence review. Am Fam Physician 2019;100:408–14.

Part III

Hair, Nail and Mucosal Diseases

13 Hair disorders (Trichoscopy)

Hair disorders (Trichoscopy)

Dermoscopy for skin of colour

Nkechi Enechukwu and Adebola Ogunbiyi

13.1 Introduction 13.1.1  Normal scalp and trichoscopy in dark skin The human hair has been classified into African, Asian, Caucasian and, recently, mixed hair types from a perspective of its biological nature and racial characteristics.1,2 Although the basic structure and physiology of the scalp and hair are similar in all racial groups,3 certain differences in the anatomic and physiologic properties are responsible for the distinctive features of the scalp and hair in persons of colour.3 This diversity in addition to the unique hair grooming practices predispose to specific hair and scalp disorders in dark-skinned patients, especially those of African descent.4–6 African hair is characterized by tightly curled, kinky hair with a tendency to form knots (type 4 hair) (Figure 13.1A); chemical hair straighteners break the cysteine disulfide bonds of the hair, thus decreasing its tensile strength and making it more pliant (Figure 13.1B).7 However, such a practice may damage the structure of the hair shaft when instructions are not adhered to.7,8 The scalp colour varies with the degree of pigmentation from light to dark brown in most individuals. A  honeycomb pigment network pattern is characteristic on trichoscopic examination (Figure 13.2), with the dark lines corresponding to the increased number of melanocytes in the rete ridge and the lighter-coloured areas corresponding to the fewer melanocytes in the supra papillary dermis.9 This pattern of pigmentation is accentuated in areas of hair loss due to sun exposure and may be discontinuous or interrupted in some forms of scarring alopecia. Regularly distributed follicular units with associated acrosyringial units are easily visualized against this background (Figure 13.2). The natural afro-textured hair is tightly curled, of intermediate thickness and elliptical or flattened in cross sectional view (Figure 13.3).10–12 Individual hair shafts are dark, maintain homogeneity in colour and are prone to twists and knots. The hair diameter varies along the length of the hair shaft (Figure  13.3). 3 There are minimal differences in the scalp shaft diameter across the genders, and the hair density in the black African is lower than that in other races.13 There are usually 3–5 number of hairs per follicular unit as is found in other racial groups. However, because of its smaller diameter, it is less dense than the other racial hair types.12 Blood vessels are not easily visualized in the darkly pigmented scalp. However, in lighter complexioned persons of colour, thin arborizing, linear and curved vessels may be seen. Asterix-like macular areas of hyperpigmentation, erythema

and scales may also be seen infrequently, whereas artifacts from hair styling products are common and manifest as brown, yellow, red or black dots or broken hairs.14 Chemical burns from hair relaxers may present as yellowish crusts with erythema and ulcerations (Figure 13.4A)

13.1.2 Scarring vs non-scarring alopecias on trichoscopy In persons of colour, an interrupted honeycomb pattern of pigmentation, absence of follicular openings, presence of fibrotic bright white dots/areas and irregularly distributed/absent pinpoint white dots (eccrine glands openings) are typical trichoscopic features of scarring alopecia (Figures 13.4B and 13.5), as none of them is classically seen in non-scarring alopecias (Figure  13.6).15 However, in scarring alopecias with sparing of the interfollicular areas (e.g., lichen planopilaris or other folliculocentric alopecias), the presence of preserved multiple pinpoint dots may make absence of follicular openings less apparent.15

13.1.3  Albino scalp The albino scalp is usually white or milky coloured and devoid of the physiological pigmented honeycomb pattern (pigment network and pinpoint white dots) observed in dark-skinned patients (Figure 13.7), whereas there are no differences between the hair texture of the natural and chemically relaxed hair of the normal pigmented individuals and albinos (Figures  13.8 and 13.9). The relative or absolute absence of pigmentation on the albino scalp makes the blood vessels easy to visualize, with thick arborizing telangiectasia resulting from photodamage often seen in males and females with either short hair or hair loss (Figure 13.7) (authors’ personal observations). The colour of the hair may vary significantly among patients, and trichoscopy may allow a better visualization. In detail, the natural colour varies from white to grey and golden brown to almost completely black depending on the degree of melanisation of the shaft (Figure 13.10), which is in turn dependent on the type of albinism and the age of the patient (as most albinos acquire some pigment in their hair with increasing age). Quite often, hair dyes are applied, thereby masking the true hair colour, yet comparison with the colour of the other body hairs determines the true hair colour. Importantly, trichoscopic features in albino subjects are similar to those seen in Caucasians, with a particular tendency to photodamage of the scalp. Nevertheless, there are some DOI: 10.1201/9780367816483-13

146

Hair disorders (Trichoscopy)

peculiarities related to the different hair shaft texture as well as racial characteristics. In general, trichoscopic findings indicating scarring (bright white areas, loss of follicular/eccrine glands openings, etc.) are difficult to visualize (Figure 13.7), whereas exogenous dark structures are easily seen because of the contrast with white hair (e.g., pediculosis – Figures 13.11

A

and 13.12) (authors’ personal observations). Additionally, hyper- and hypopigmented clues are often absent (“peripilar sign”, “starry sky-like” pattern, perifollicular white scales, perifollicular fibrosis, etc.) because of the pigmentation deficiency and the lack of contrast, respectively (authors’ personal observations)

B

FIGURE 13.1  African natural hair: tightly curled, kinky hair with a tendency to form knots (type 4 hair) (A). African hair treated with chemical straighteners (B).

A

B

FIGURE 13.2  Honeycomb pigment network is characteristic of the scalp of dark-skinned patients on trichoscopy (A). Regularly distributed follicular units along with acrosyringial ostia (seen as white dots) are easily visualized against the dark background (B).

147

Dermoscopy for skin of colour A

B

FIGURE 13.3  Natural afro-textured hair: tightly curled black hairs that are elliptical or flattened in cross-sectional view (A). African hair is homogeneous in colour but the diameter may vary along the length of the hair shaft; twists and knots are also commonly seen (B).

A

B

FIGURE 13.4  Yellowish crusts caused by chemical burns from hair relaxers (A). Interrupted honeycomb pattern of pigmentation along with reduction of follicular openings and eccrine glands openings (pinpoint white dots) are indicative of scarring alopecia (B).

A

B

FIGURE 13.5  Trichoscopic images of scarring alopecias. Besides disruption of the brown honeycomb and reduction of the follicular/eccrine glands openings, there are also bright white areas (corresponding to dermal fibrosis), including lines (A) and structureless areas (B).

148

Hair disorders (Trichoscopy) A

B

FIGURE 13.6  Trichoscopic images of non-scarring alopecias. Brown honeycomb pattern and follicular/eccrine glands openings are preserved; no fibrotic bright white area is present (A, B).

A

B

FIGURE 13.7  Trichoscopy in albinism affecting African patients. Lack of the honeycomb pigment network pattern and pinpoint white dots (eccrine ostia) (A, B). Unfocused branching/reticular vessels and white structureless areas resulting from photodamage in a case of long-standing alopecia (B).

A

B

FIGURE 13.8  Albino patient of African descent (A). Trichoscopy shows the white colour of the hair shafts, which appear tightly curled (B).

149

Dermoscopy for skin of colour A

B

FIGURE 13.9  Chemically relaxed hair in an African patient with albinism (A). Trichoscopy shows the absence of the honeycomb pigment network pattern and no visible pinpoint white dots (B).

A

B

C

D

FIGURE 13.10  Trichoscopy allows a better visualization of the hair colour of African albino patients, with shade varying from white (A) to golden (B) and grey (C) to almost completely black in rufous albinism (D).

A

B

FIGURE 13.11  Pediculosis in a young adult African female with oculocutaneous albinism (A). Dermoscopy highlights a live louse, which is prominent against the lighter-coloured scalp and white hair shaft (B).

150

Hair disorders (Trichoscopy) A

B

FIGURE 13.12  Trichoscopy of pediculosis in an African albino patient. Non-viable nit displaying a grey colour and a flattened end (A). Viable nit presenting as oval black/dark grey structure (B).

13.2  Non-scarring alopecias 13.2.1  Androgenetic alopecia – introduction Androgenetic alopecia (AGA) is the most common form of hair loss seen in men and women globally,15 yet its prevalence is lower in Africans compared with that in Caucasians and Asians.16 It is a genetically determined patterned hair loss causing progressive follicular miniaturization and alteration in the hair cycle dynamics through the effects 5α-dihydrotestosterone (DHT) on the dermal papilla of the hair root.15,16

13.2.2 Androgenetic alopecia – clinical presentation Hair loss in AGA is patterned in both men and women, with the frontotemporal area and vertex being more commonly involved in the former (Figure  13.13A) and hair loss mainly affecting the parietal areas and vertex with retention of the frontotemporal line being typical of the latter.17,18 Thinning and loss of hair is asymptomatic and progresses over time; the main differential diagnosis in skin of colour includes central centrifugal cicatricial alopecia.17,18

13.2.3  Androgenetic alopecia – trichoscopy The earliest trichoscopic feature consists in the miniaturization of the hair shaft leading to a variation in hair shaft diameter affecting more than 20% of the follicles (hair shaft thickness heterogeneity) (Figure  13.13B).19 Additionally, there is an increase in vellus hairs along with a decrease in the number of hairs in the follicular units, with many units having single hairs (Figure 13.13B); short and thin (0.003 mm in diameter) regrowing hairs are also commonly seen in the frontal area.19,20 Notably, a rim of pigmentation (the so-called “peripilar” sign), corresponding to perifollicular inflammation on histology,9 is often seen around the follicular opening in dark skin, whereas the honeycomb pigmented network is usually intact with regularly distributed pinpoint white dots (eccrine

glands) (Figure  13.14A); other (non-perifollicular) macular hyperpigmented areas may be seen.21 Features seen in more severe forms include white dots (empty follicles), yellow dots (Figure 13.14B) and interfollicular scales.9,19–21 Importantly, the honeycomb pigment network and “peripilar” sign are typically absent in albino patients, with hyperkeratotic yellow dots and miniaturized hairs being the main diagnostic clues in such subjects (Figures  13.15 and 13.16A) (authors’ personal observations). Additionally, hair shaft diameter heterogeneity is difficult to ascertain in the early phases (Figure 13.15), and skin photodamage signs are often seen in long-standing cases (Figure 13.16B) (authors’ personal observations).

13.2.4  Alopecia areata – introduction Alopecia areata (AA) is a chronic autoimmune disease characterized by non-scarring patchy hair loss affecting the scalp hair or other body hairs that is reportedly more common in blacks.22 The pathogenesis is unclear, yet certain mechanisms involving a complex interaction between genetic susceptibility genes, loss of immune privilege and immune dysregulation have been suggested.23,24

13.2.5  Alopecia areata – clinical presentation There are several clinical variants depending on the pattern of hair loss (Figures 13.17A and 13.19A–13.21A). The patchy variant is most common and manifests as single or multiple roundish alopecic patches (Figure  13.17A), which are frequently misdiagnosed as tinea capitis.24 Patchy AA may progress to involve the whole scalp hair (AA totalis) or the body hairs (AA universalis) (Figures  13.20A and 13.21A).24 Other variants include the ophiasis pattern (affecting the occipital scalp) and sisaipho (ophiasis inversus  – involving the frontal, temporal and parietal scalp).24 The eyebrows, eyelash, beard, pubic and other body hairs (Figure 13.19A) may also be affected and nail abnormalities (e.g., regular nail pits and trachyonychia) may also be seen.24

151

Dermoscopy for skin of colour

13.2.6  Alopecia areata – trichoscopy Trichoscopic features of AA vary based on the disease duration and severity. As with other forms of non-scarring alopecias, there is a preservation of the normal honeycomb pigmented network pattern (Figures 13.17B–13.21B).9,15,21,25–27 Yellow dots are infrequent and not easily visualized in persons of African descent when compared with visualization in Asians or Caucasians, whereas micro-exclamation mark hairs (hair displaying a progressive thinning of the shaft towards the base) are commonly seen (Figure 13.18A), especially in active disease, but they are not absolutely pathognomonic.9,15,21,25–27 Other possible findings observed in AA include black dots (cadaverized hair), tapering hairs, broken hairs and clustered vellus hairs (Figure 13.17B–13.21B).9,15,21,25–2 In a single large study carried out among Asians, yellow dots and short vellus hairs were the most sensitive markers, whereas black dots, tapering hairs and broken hairs were the most specific markers for diagnosis.27 Yellow dots, black dots and short vellus hairs were found to be linked to disease severity, whereas black dots, tapering hairs, broken hairs and short vellus hairs correlated with disease activity.27 Upright regrowing hairs, pigtail hairs (circle hairs) (Figures 13.17B and 13.18B), grey intermediate vellus hairs (Figure  13.20B) and partially pigmented hairs are often seen during the regrowth phases.9,15,21,25–27 In alopecia totalis or universalis, the hair may be totally absent with accentuation of the pseudonetwork pigmentation pattern (Figure 13.21B).9,15,21,25–27

13.2.7  Tinea capitis – introduction Tinea capitis is a fungal infection of the hair/scalp mainly affecting children and caused by the fungal species Trichophyton and Microsporum.28 There are three clinical subtypes, including non-inflammatory forms (commonly caused by anthropophilic fungi), inflammatory forms (frequently related to zoophilic or geophilic fungi) and tinea favosa (favus – caused by Trichophyton schoenleinii).28–30

13.2.8  Tinea capitis – clinical presentation The clinical features of tinea capitis vary with clinical types. Among the non-inflammatory forms, the “grey patch” type is the commonest variant and presents as single or multiple patches of focal hair loss with scales (Figure 13.22A), whereas the “black dot” and “seborrheic” types respectively manifest as areas of hair loss with broken hairs appearing as black dots (Figure  13.23A) and subtle hair loss and diffuse scale.30,31 Kerion represents a pattern of inflammatory tinea capitis presenting with an inflamed boggy pus-filled mass or multiple pustules in an erythematous background, whereas tinea favosa is typified by more or less diffuse hair loss along with a mixture of crusts, debris and fungal hyphae giving rise to the characteristic yellowish-white “scutula” (Figure 13.24A).30,31 Notably, both kerion and favus may progress to scarring hair loss.30

13.2.9  Tinea capitis – trichoscopy The hallmark of tinea capitis is the comma hairs and corkscrew hairs, with the latter being more common in dark-skinned

patients (especially African people) (Figures  13.22B and 13.23B).30 Other common but not specific findings of tinea capitis include black dots, perifollicular and interfollicular scales, regrowing hairs, bent hairs and zig-zag hairs (Figures 13.22B, 13.23B and 13.25).31–33 Notably, white sheaths around the proximal hair shaft also have been observed in skin of colour, whereas “Morse code” hairs (Figure 13.25) (hairs displaying horizontal white bands corresponding to empty bands related to localized areas of fungal infection that are considered characteristic of tinea capitis) are less frequent when compared with the incidence in whites.31,34–36 Erythema, follicular pustules, black dots, zig-zag hairs and structureless areas devoid of hair follicular openings are commonly found in kerion, yet more specific features (e.g., “comma”, “corkscrew” and “Morse code” hairs) may also be observed.30,37 Finally, broken hairs along with sulphur-yellow crust and areas devoid of follicular opening are seen in favus (Figure 13.24B).30,37

13.2.10  Trichotillomania – introduction Trichotillomania is a particular form of traction alopecia resulting from habitual, repetitive removal of one’s own hair.38

13.2.11  Trichotillomania – clinical presentation It is clinically characterized by single or multiple patches of irregular hair length or hairless areas (Figure 13.26A).38

13.2.12  Trichotillomania – trichoscopy The most common trichoscopic feature of trichotillomania is the presence of hair shafts broken at different lengths and displaying a variable shape (Figure  13.26B).38 From a morphological point of view, the broken hairs appear as short hairs with trichoptilosis (longitudinal splitting of the hair shafts), coiled hairs (short hairs irregularly coiled at the distal ends), hook hairs (partially coiled short hairs), flame hairs (semitransparent, wavy, cone shaped), or tulip hairs (short hairs with a darker, tulip-shaped end, which looks empty inside) (Figure 13.26B).38 Additional trichoscopic findings include the so-called “V-sign” (two or more short hairs in one follicular unit, broken at similar levels), black dots (hairs are fractured at the level of the scalp surface) and hair powder (sprinkled hair) (Figure 13.26B).38

13.2.13  Traction alopecia – introduction Traction alopecia is an acquired form of traumatic hair loss resulting from prolonged repetitive tension on scalp hairs mostly because of excessive hairstyling practices.39 It is reversible in the early phases, yet repeated traction over time may lead to permanent hair loss.40 Traction alopecia is commonly seen in African women and children because of hair styling practices involving pulling on the scalp hairs (e.g., weaves, twists, braids and cornrows), use of tight African head scarfs and intrinsically geometric weak points typical of persons of African descent.41–45

152

Hair disorders (Trichoscopy)

13.2.14  Traction alopecia – clinical presentation

13.2.17  Telogen effluvium – clinical presentation

Hair loss in traction alopecia may present acutely within a few weeks of hair styling or it may be gradual in onset.45–46 The commonest site of involvement is the frontotemporal region (Figures 13.27A–13.30A), making it a frequent cause of marginal alopecia, although other scalp areas subjected to repetitive tension may be involved, such as the occipital and vertex regions.45–46 Early features of traction alopecia include loss of hair, scalp tenderness, erythema, papules and pustules, with the last two findings being particularly common in children (traction folliculitis) (Figures  13.27A and 13.28A).45–46 Hair loss is usually reversible in the early phases, whereas irreversible hair loss of the terminal hairs is typical of chronic stages;45–46 the “fringe sign” is visible in long-standing cases, in which shorter hairs not put under tension remain at the hair margins (Figures 13.27A–13.30A).47

Telogen effluvium presents with diffuse hair shedding associated with hair thinning involving the whole scalp (Figure 13.33A).48–50 There may be a history of an antecedent inciting factor that occurred 3–4 months earlier.48–50 In chronic forms, hair loss may continue for 6–8 months. Gentle hair pull will often be strongly positive in active cases.48–50

13.2.15  Traction alopecia – trichoscopy Trichoscopy findings of traction alopecia vary with clinical stages, with early features being erythema, pustules, crusting, broken hairs and, most importantly, peripilar hair casts (often surrounded by fibrotic perifollicular bright white halos in the intermediate phases of the disease) (Figure 13.27B); the pigment pseudonetwork is often intact and pinpoint white dots are usually visible and regularly spaced (Figure  13.29B).21 Notably, hair casts are less evident in albinos (Figures  13.31 and 13.32A) and in grey hairs.21 In older lesions, fibrotic bright white dots, broken hairs, irregularly distributed pinpoint white dots (eccrine glands openings), interfollicular hyperpigmentation and miniaturized hairs (damaged, thinned hairs) are seen (Figures 13.28B and 13.30B).21 Peripilar hair casts at this stage are infrequent, whereas vellus hairs are typically preserved and regrowing hairs may be apparent.21 Of note, in contrast to what is seen in pigmented individuals, fibrotic white dots or peripilar halos as well as perifollicular and interfollicular hyperpigmentation are generally not seen in albino subjects, whereas sun-induced unfocused vessels are often evident in long-standing cases (Figure 13.32B) (authors’ personal observations).

13.2.18  Telogen effluvium – trichoscopy The trichoscopic findings in telogen effluvium in skin of colour are not specific, similar to what is observed in fair-skinned patients.15,50 Consequently, diagnosing such a condition is a process of exclusion.15,50 The most characteristic dermoscopic clue of telogen effluvium is the lack of findings typical of other conditions.15,50 Common, but non-specific, features include empty hair follicles, predominance of follicular units with only one hair, perifollicular discolouration (peripilar sign), yellow dots, upright regrowing hairs (mainly acute forms) and progressive uniform hair thinning (chronic forms) (Figure 13.33B).15,50 The presence of