in pigmented skin

CLINICALDERMATOLOGY

INPIGMENTEDSKIN Volume 1

RanthilakaR.Ranawaka

Clinical Dermatology in

Pigmented Skin Volume I

Ranthilaka R. Ranawaka

Clinical Dermatology in Pigmented Skin

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COPYRIGHT & REPRODUCTION All rights reserved. No part of this publica on may be reproduced or transmi ed in any form or by any means electronic or mechanical, including photocopying or any informa on storage and retrieval system without wri en permission of the author. Dr Ranthilaka R. Ranawaka MBBS (Colombo) MD (Dermatology) Consultant Dermatologist, General Hospital Kalutara, Sri Lanka. [email protected] September 2017

ACKNOWLEDGEMENT I thank Dr Priyanka H. Abeygunasekara MBBS DPath MD Path (Histopath), Consultant Pathologist at Na onal Ins tute for Cancers, Sri Lanka, for assis ng me with histopathology reports, and Dr. Shalindra Ranasinghe MBBS (Colombo) M.Phil (Keele) PhD (SJP), Head/Department of Parasitology, Faculty of Medical Sciences, University of Sri Jayewardenepura, Sri Lanka, for her valuable contribu on with leishmaniasis microscopy slides. Dr Ranthilaka R. Ranawaka

Printed by

Ananda Press 277, Hokandara Road, Thalawathugoda, Sri Lanka. [email protected]

ISBN No: 978-955-38441-0-1 ii


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INTRODUCTION This book illustrates unusual presenta ons of common skin diseases in tropics. Over 30 disease en es are discussed and the answers are given with a brief descrip on of the disease and the related dermatoses with over 125 colour illustra ons. This is the first illustrated dermatology atlas done solely with Sri Lankan pa ents. This book has been wri en by a clinician for clinicians, to provide a clear and easy guide to iden fy common skin diseases prevalent in tropics. Although there are many atlases in dermatology, which are of dermatoses in pigmented skin is lacking. Common skin diseases such as psoriasis, lichen planus, eczema, and erythrasma are darker in pigmented skin. For example, in PASI (Psoriasis Area Severity Index) erythema is always 0 or 1; lichen planus is blackish rather than pinkish; erythrasma is never erythematous; lichen amyloidosis is blackish; in darker skin. Therefore it is important that dermatology trainees and general prac oners trea ng pa ents of coloured skin (Fitzpatrick type V) to use an atlas with own pa ents to get familiar with this diverse clinical presenta ons. Tropical diseases such as cutaneous tuberculosis, leishmaniasis, deep fungal infec ons, oral submucous fibrosis etc are not uncommon in our rou ne skin clinics. This atlas meant to s mulate the interest in tropical dermatology in dermatology trainees, general prac oners, and dermatologists from non-tropical countries.

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Dr Ranthilaka R. Ranawaka MBBS MD (Dermatology) is currently holding the post of consultant dermatologist a ached to Ministry of Health Sri Lanka. She qualified MBBS in 1996 and MD Dermatology in 2004 from University of Colombo, Sri Lanka. She had one year training in clinical trials conducted on psoriasis and acne at St John’s Ins tute of Dermatology, London, UK in 2006. She has published 26 scien fic papers in na onal and interna onal journals including six clinical trials. She presented more than 60 abstracts in na onal and interna onal conferences. She is an author of “100 cases of Leprosy”, “Guidelines in the Management of Leishmaniasis in Sri Lanka” and “The Global Atlas of Dermatology, Venereology and Leprology”. Her main areas of research interest are leishmaniasis, cutaneous tuberculosis, onychomycosis and leprosy. She is an Editorial Board Member in The Journal of Procedural Dermatology, PiscoMed Publishing Pte Ltd – since 2015, and an Academic Editor of the Interna onal Journal of Tropical Disease and Health. Dr Ranthilaka is a reviewer in number of indexed journals; Interna onal Journal of Dermatology, Bri sh Journal of Dermatology, Clinical and Experimental Dermatology, Mycopathologia, Indian Journal of Pharmacology, Bri sh Journal of Medicine and Medical Research, Indian Journal of Dermatology and Indian Journal of Dermatology, Venereology and Leprology. She is a guest speaker in local and South Asian dermatology conferences. She was awarded number of travel awards (AAD 2006, EADV 2006, WCD 2007, ICD 2009) and research awards including European Nail Research Grant in 2008, SLMA-FairMed research grant in 2012 and 2014. She was awarded President's Award for Scien fic Publica ons in 2009, 2010, 2011, 2015 and 2016, and was among top ten researchers in 2009.

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CONTENTS Introduc on

iii

Acknowledgement

iv

Ques ons with illustra ons

1-20

Answers with illustra ons

22 - 87

(1)

Cutaneous leishmaniasis

22

(2)

Cutaneous tuberculosis

28

(3)

Chromoblastomycosis

34

(4)

Impe go

36

(5)

Fungal infec ons

38

(6)

Intertriginous candidosis

46

(7)

Becker naevus

49

(8)

Lip lick derma

(9)

Cutaneous larva migrans

s

49 50

(10) Cutaneous horn

52

(11) Scabies

54

(12) Fish tank granuloma

55

(13) Oral submucous fibrosis

56

(14) Acanthosis nigricans

58

(15) Allergic contact derma

s

60

(16) Halo naevus

63

(17) Leprosy

64

(18) Vi ligo

69

(19) Pigmentory mosaicm

73

(20) Squamous cell carcinoma

74

(21) Basal cell carcinoma

76

(22) Lichen striatus

79

(23) Erythrasma

80

(24) Photodermatoses

82

(25) Acroderma

86

s enteropathica

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A farmer living in Anuradhapura (North Central province in Sri Lanka) presented with an asymptoma c ulcer on his right breast for three months. He was treated several mes with oral and topical an bio cs with poor response. a) What is your clinical diagnosis ? b) What are the clinical criteria to diagnose this condi on in an endemic area ? c) How do you confirm the disease ? d) What are the treatment op ons ?

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Figure 2a: Classical tuberculous histology without casea on. (H&E X10) (Courtesy Dr. Priyanka H. Abeygunasekara, Consultant Pathologist at Na onal Ins tute for Cancers, Sri Lanka)

Figure 2b: Classical tuberculous histology with unremarkable epidermis and upper dermis containing granulomata composed of collec ons of epithelioid cells, Langerhan type giant cells, his ocytes and moderate infiltrate of lymphocytes without casea on. (H&E x 40) (Courtesy Dr. Priyanka H. Abeygunasekara, Consultant Pathologist at Na onal Ins tute for Cancers, Sri Lanka)

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A 36 year-old farmer presented with a scaly growth on his right wrist for six months. This was asymptoma c. No lesions elsewhere in the body. a) What are your differen al diagnoses? b) How do you differen ate? c) Fig 2a and 2b shows the histopathology of the lesion. What is your diagnosis? d) What is the treatment?

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Figure 3a: Chromomycosis: granulomatous response (H&E, x10) (Courtesy Dr Priyanka H. Abeygunasekara, Consultant Pathologist at Na onal Ins tute for Cancers, Sri Lanka)

Figure 3b: Chromo spores in higher magnifica on (H&E, x40) (Courtesy Dr Priyanka H. Abeygunasekara, Consultant Pathologist at Na onal Ins tute for Cancers, Sri Lanka)

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A 25 year-old woman presented with an asymptoma c warty growth on her right knee for more than three years. She has not sought treatments and the lesion had slowly progressed over years. a) What are your differen al diagnoses? b) How do you differen ate? c) Fig 3a and 3b shows the histopathology of the lesion. What is your diagnosis? d) What is the treatment?

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A child presented with fever and blistering erup on for one week. a) What is your diagnosis? b) What are the possible complica ons if treatment is delayed? c) How do you treat this condi on?

(5) A 35 year-old house wife presented with itchy scaly lesion on the le palm for 2 months. a) What is your probable diagnosis? b) How do you confirm? c) What is the treatment?

(6) A 57 year-old woman complained of burning sensa on of her palms. a) What is your clinical diagnosis? b) What are the predisposing factors? c) What advice would you give to the pa ent?

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A 17 year-old boy is worried about this pigmented patch on his R/shoulder which enlarges progressively. a) What is your diagnosis? b) How do you reassure him? c) What are the treatment op ons available?

(8) A 17 year-old girl complained of pigmenta on around her mouth. a) What is your diagnosis? b) What advice would you give to the pa ent?

(9) A 9 months-old child presented with a very itchy lesion on the back of the trunk. His mother had no ced that the linear lesion is gradually moving forward. a) What is your clinical diagnosis? b) What are the causa ve organisms? c) How do you treat the condi on?

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A 45 year-old woman came with this asymptoma c growth. a) What is your diagnosis? b) Why excision with histopathology is essen al?

(11) A 21 year-old girl came with this itchy rash on hands and body. Her 19 year-old sister also had similar complaint. a) What is your diagnosis? b) What advice would you give to her family members?

(12) A young man who involved in aquaculture (fish farming) came with a warty lesion on the right hand for more than six months. a) What is your clinical diagnosis? b) What are the causa ve organisms? c) Why is he having mul ple nodules? d) How do you treat this condi on?

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A young man presented with hypopigmenta on of his lips for six months dura on. a) What are your differen al diagnoses? b) How do you differen ate clinically? c) What are the predisposing factors? d) How do you confirm your diagnosis?

(14) A 15 year-old girl's mother is worried that the child is ge ng dark, thickened skin around her neck. a) What is your diagnosis? b) What other related clinical features she has in this photograph? c) What inves ga ons would you suggest in this girl?

(15) A 40 year-old woman complained of an itchy rash on her back which did not cure with topical steroids prescribed by her GP. a) Why is this skin problem recurring? b) What is vital in examina on? c) What advice would you give to the pa ent?

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(16) The mother of this girl is worried about this skin lesion. a) What is your diagnosis? b) W h a t o t h e r s k i n problem/s can co-exist?

(17) A 23 year-old mother of one child complained of this non itchy, tender, erythematous plaque which appeared within few days. She denied sensory impairment. a) What is your differen al diagnosis? b) How do you confirm your diagnosis? c) She is breast feeding her one year-old child and is worried about taking oral medi-ca ons. What advice would you give her?

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What is this clinical condi on?

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1) What is your diagnosis? 2) What advice would you give to this child's parents?

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(20) A 5 5 y e a r- o l d m a n complained of a warty growth on his right flank on top of an old burn scar. a) What inves ga on would you suggest, and why?

(21) a) What is your clinical diagnosis? b) What are the treatment op ons? c) T h i s w o m a n h a s m u l p l e s e b o r rhoeic keratoses and DPN (dermatosis papulosa nigra) on her face too. What treatments would you suggest for them?

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(22) The mother of this child is worried that a linear lesion is growing along his right upper limb for last few weeks. a) What is your diagnosis? b) What advice would you give to the mother ?

(23) A 52 year-old man came with this pigmented patch in his axillae bilaterally. a) What is the diagnosis? b) Where else would you like to examine? c)

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A 72 year-old man complained of itchy rash on sun exposed areas. a) What is your diagnosis? b) What is most important in management?

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A 4 months old baby girl was brought with a non-itchy eczematous rash. She also had similar rash around the mouth and neck creases. a) What is the probable diagnosis? b) How do you confirm it? c) What advice would you give the mother regarding the treatments?

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Answers The answers are given with a brief description of the disease and further illustrations and descriptions on the related dermatoses.

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(1) a) Cutaneous leishmaniasis (nodular-ulcera ve lesion is the most common clinical form in Sri Lanka). b) In endemic areas of the world any boil that is present for several weeks and does not respond to ordinary therapy should be considered as CL unless proven otherwise. c) Slit skin smear for amas gotes, skin biopsy showing LD bodies, culture, PCR. d) In Sri Lanka sodium s bogluconate (intralesional, IM or IV) and liquid nitrogen cryotherapy are widely used.

Cutaneous leishmaniasis Protozoal disease transmi ed by sandfly vectors. There are several species of leishmanisis, each occupying a par cular zoogeographical zone. The disease is endemic in 88 countries, most commonly in tropical and subtropical regions. Manifesta ons of disease range from cutaneous ulcers to systemic mul organ disease. In Sri Lanka leishmaniasis is mostly prevalent in North Central and Southern provinces. The causa ve organism has been iden fied as Leishmania donovani zymodeme MON-37. The diagnosis of CL largely depends on the clinical appearance, especially in endemic areas. As a general rule in endemic areas of the world any boil that is present for several weeks and does not respond to ordinary therapy should be considered as CL unless proven otherwise.

Inves ga ons 1. D e m o n s t ra o n o f a m a s g o t e s i n Giemsa-stained smears from infected skin by direct microscopy. 2. Demonstra on of intracellular amasgotes in the dermis of H & E sec ons of skin. 3. Presence of leishmanial granulomas in the dermis in H & E specimens. 4. Growth of promas gotes in Nicolle– Novy–MacNeal (NNN) culture medium from lesional specimens. 5. Demonstra on of leishmanial DNA by PCR. Treatments I n S r i L a n ka s o d i u m s b o g l u co n ate (intralesional, IM or IV) and liquid nitrogen cryotherapy are widely used. Several studies have been conducted and proven efficacy of heat therapy, hypertonic saline and intralesional metronidazole as alterna ve therapies.

References 1. Karunaweera ND, Pratlong F, Siriwardane HVYD, Ihalamulla RL, Dejet JP. Cutaneous leishmaniasis is caused by Leishmania donovani zymodeme MON-37. Transacon of the Royal Society of Tropical Medicine and Hygiene 2003; 97: 380-1. 2. Ranawaka RR, Weerakoon HS, de Silva SH. Randomized double-blind, controlled, compara ve study on intralesional 10% and 15% hypertonic saline versus intralesional sodium s bogluconate in Leishmania donovani cutaneous leishmaniasis Int J Dermatol. 2015;54(5):555-63. 3. Ranawaka RR, Weerakoon HS, Opathella N. Liquid nitrogen cryotherapy on Leishmania donovani cutaneous leishmaniasis. Journal of Dermatologic Treatment 2011; 22: 241-5. 4. Ranawaka RR, Abeygunasekara PH, Weerakoon HS. Correla on of clinical, parasitological and histopathological diagnosis of cutaneous leishmaniasis in an endemic region in Sri Lanka. Ceylon Medical Journal. 2012;57(4):14952. 5. Refai Refai FW, Madarasingha NP, Fernandopulle R, Karunaweera N. Nonresponsiveness to standard treatment in cutaneous leishmaniasis: A case series from Sri Lanka. Trop Parasitol. 2016 Jul-Dec;6(2):155-158. 6. Rathnayake D, Ranawake RR, Sirimanna G, Siriwardhane Y, Karunaweera N, De Silva R. Co-infec on of mucosal leishmaniasis and extra-pulmonary tuberculosis in a pa ent with inherent immune deficiency. Int J Dermatol. 2010 May;49(5):549-51

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Figure 1.1: Cutaneous leishmaniasis has many clinical forms; (a) papules and (b) plaques are common.

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Figure 1.2: Cutaneous leishmaniasis can mimic (a) psoriasis (b) tropical ulcer.

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Figure 1.3: When cutaneous leishmaniasis occurs (a) on car lages and (b) at the angle of the eye, management would be difficult with local treatments; such as with intralesional injec ons, liquid nitrogen cryotherapy or heat therapy. The lesion in figure (b) mimics basal cell carcinoma on face.

Figure 1.4: Nodulo-ulcera ve lesions as shown in this pa ent are the most common clinical presenta on in cutaneous leishmaniasis. Depigmented halo around CL (as shown in this case) is documented in pigmented skin.

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Figure 1.5: (a) A nodular – ulcera ve lesion of CL. (b) Post inflammatory hypopigmenta on is common with liquid nitrogen cryotherapy which re-pigments spontaneously within 6-8 months.

Figure 1.6: When post inflammatory hypopigmenta on occurs on the face it becomes a cosme c and a social problem un l it re-pigment spontaneously.

Figure 1.7: Leishmania recidivans around a healed CL scar.

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Figure 1.8: Slit Skin Smear (SSS) stained with Giemsa (x 1000 magnifica on) showing macrophages filled with Leishmania amas gotes. Black arrow:macrophage nucleus, Red arrow: Leishmania amas gotes with dot (nucleus) and dash (kinetoplast) appearance (Courtesy Dr. Shalindra Ranasinghe, Head/Department of Parasitology, Faculty of Medical Sciences, University of Sri Jayewardenepura, Sri Lanka) 1

2

3

4 5

6

7

8

9 10 11 12 13 14

500bp 120bp

Figure 1.9: Polymerase Chain Reac on (PCR) of DNA extrac ons from punch biopsy samples of slit skin smear (SSS) posi ve cutaneous lesions. DNA was amplified with JW 11 &12 primers (Rogers et al. 1987). Lane 1: 100bp DNA ladder (marker), Lane 2: pa ent sample 1, Lane 3: pa ent sample 2, Lane 4: pa ent sample 3, Lane 5: pa ent sample 4, Lane 6: pa ent sample 5, Lane 7: pa ent sample 6, Lane 8: pa ent sample 7, Lanes 9-11 empty wells with no samples. Lane 12: -ve control with no DNA, Lane 13: +ve control with DNA of Leishmania culture. Gel electrophoresis was captured under UV light a er staining with ethidium bromide. Different intensi es of bands were seen according to the quan ty of Leishmania DNA available in the sample. (Courtesy Dr. Shalindra Ranasinghe, Head/Department of Parasitology, Faculty of Medical Sciences, University of Sri Jayewardenepura, Sri Lanka) References: Rogers WO, Wirth DF 1987. Kinetoplast DNA minicircles: regions of extensive sequence divergence. Proc Natl Acad Sci U S A 84: 565-69

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Figure 1.10: Mucocutaneous leishmaniasis; ulcer on mucosa not respond to conven onal treatment should alert clinicians in an endemic area.

Figure 1.11: Mucocutaneous leishmaniasis; A 54 year-old farmer was inves gated since 2004 for non-healing ulcer on the lower lip for more than three years. Repeated histology showed granulomatous inflamma on without casea on or LD bodies. In 2007, PCR was posi ve for leishmaniasis; and was treated with intra muscular sodium s bogluconate. By that me his lower lip, hard palate and the nasal septum were destructed and re-construc on surgery was performed. He had concomitant TB lymphadeni s making the diagnosis more complex as both diseases show granulomatous inflamma on in histopathology.

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(2) a) Chromoblastomycosis / Lupus vulgaris b) Skin biopsy - Classical tuberculous histology with unremarkable epidermis and upper dermis containing granulomata composed of collec ons of epithelioid cells, Langerhan type giant cells, his ocytes and moderate infiltrate of lymphocytes without casea on (figures 2a & 2b). c) Lupus vulgaris d) An TB drugs for six months

Cutaneous tuberculosis Cutaneous infiltra on of tuberculosis (TB) occur through, direct inocula on, autoinocula on, haematogenous spread or contagious spread. The wide clinical spectrum of cutaneous TB is dependent on the route of infec on, the immune status of the pa ent and the previous sensi za on with TB. Diagnosis Cutaneous TB is best diagnosed using a comprehensive work up of the pa ent in which histologic study of the skin biopsy specimen is most essen al. Mantoux reac vity, TB culture, or the erythrocyte sedimenta on rate (ESR) although posi ve results facilitate clinical diagnosis, nega ve results do not exclude TB (Ramam et al 2011, Ranawaka RR et al 2010). Polymerase chain reac on (PCR) has emerged as a promising tool in the diagnosis of cutaneous TB and atypical mycobacteria infec ons. More recently, a new diagnos c method, interferon-gamma enzyme-linked immunosorbent assay (Quan FERON TB-gold in tube, (QFT-2G), has been developed to detect latent tuberculosis infec on.

Treatments First line an -TB drugs (CAT1) are given for six months: i.e. isoniazid ( H) 10mg /kg , rifampicin(R) 10mg/kg, pyrazinamide (Z) 30mg/kg and ethambutol (E) 15mg/kg (HRZE). All 4 drugs are given for the first two months, followed by isoniazid and rifampicin for the next four months. Second line an TB drugs (CATII) are HRZE plus intramuscular streptomycin 500 mg to 1g daily for 60 days, followed by HRZE for 1 month and HR for another 5 months. In our case series of 20 pa ents, 16 of them showed total disappearance of the skin lesion within six weeks of an TB therapy (Ranawaka RR et al 2010). Therefore an alterna ve cause should be considered if the clinical response to an -TB drugs is unapparent within six weeks (Ramam and Ramesh 2010).

References 1. 2. 3.

4. 5. 6.

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Atukorala DN, Amerasekera LR (1988). Tuberculosis of the skin in Sri Lanka. Ceylon Med J ;33(3):97-9. Padmavathy L, Lakshmana Rao L, Pari T, Ethirajan N, Krishnaswamy B (2008). Lupus vulgaris and tuberculosis verrucosa cu s - a clinical, pathological and epidemiological study of 71 cases. Indian J Tuberc ;55(4):203-209. Ramam M, Malhotra A, Tejasvi T, Manchanda Y, Sharma S, Mi al R, Ramesh V (2011). How useful is the Mantoux test in the diagnosis of doub ul case of cutaneous tuberculosis ? Int J Dermatol. 50(11):1379-82. doi: 10.1111/j.1365-4632.2011.04971. Ramam M, Ramesh V (2010). Trial of an tubercular therapy in the diagnosis of cutaneous tuberculosis. Am J Dermatopathol. 32(3):316. doi: 0.1097/DAD.0b013e3181c6ed81 Ranawaka RR, Abeygunasekara PH, Perera E, Weerakoon HS (2010). Clinico-histopathological correla on and the treatment response of 20 pa ents with cutaneous tuberculosis. Dermatol Online J. 16(8):13. Yates VM and Walker SL (2016) Mycobacterial Infec ons. Rook's Text Book of Dermatology, 9th Edn, WileyBlackwell Science, UK, p 27.6


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Figure 2.1: A 48 year-old woman who was on oral dexamethasone pulse for two years for her mixed connec ve ssue disease; with lupus vulgaris (a) before treatment, (b) complete resolu on of the lesion with a scar a er five months of an TB therapy.

(a)

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Figure 2.2: A 40 year-old woman with lupus vulgaris (a) before treatment, (b) complete resolu on of the lesion without a scar a er two months of an TB therapy.

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Figure 2.3: Lupus vulgaris; (a) before treatments (b) total clearance of the lesion without a scar a er eight weeks of an TB therapy. Post inflammatory pigmentory changes disappear spontaneously within 6 to 8 months.

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Figure 2.4: A 25 year-old woman with (a) tuberculosis verrucosa cu s (warty TB) on le index finger, (b) reduced in size a er skin biopsy. This is a well recognized clinical response.

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Classifica on of Cutaneous TB (Yates and Walker 2016) Host immunity

Method of inocula on

Disease manifesta on

Normal

Direct inocula on

Tuberculous chancre

Low Low Low Low

Contagious spread Autoinocula on Haematogenous spread Haematogenous spread

Scrofuloderma Orificial TB Acute miliary cutaneous Tuberculous gumma

High High High High

Direct inocula on Direct inocula on Haematogenous spread ? Haematogenous spread

Warty TB (tuberculous verrucosa cu s/ TVC) Lupus vulgaris Lupus vulgaris Tuberculids Lichen scrofulosorum Papulonecro c tuberculid Erythema induratum (Bazin's)

Figure 2.5: A 61 year-old man with lupus vulgaris (a) before treatment, (b) good clinical response a er two months of an TB therapy. This lesion healed with residual scarring.

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Figure 2.6: A 33 year-old man with warty TB on his right knee (a) before therapy, (b) more than 90% clinical improvement a er three months of an TB therapy.

Figure 2.7: Warty TB totally disappeared without a scar one month a er an TB therapy.

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Figure 2.8: (a) A 70 year-old woman came with an asymptoma c erythematous plaque on her face for two months. She developed this lesion while she was on an TB (CAT 1) therapy for TB lymphadeni s. Skin biopsy from the skin plaque revealed cutaneous infiltra on of TB. (b) Con nua on of an TB drugs cured her skin lesions completely without a scar.

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(3) a) Chromoblastomycosis/ Warty tuberculosis (TVC) b) Skin biopsy – Fig (2a) granulomatous response (H&E, x10), Fig (2b) Chromo spores in higher magnifica on (H&E, x40) c) Chromoblastomycosis d) Liquid nitrogen cryotherapy ± itraconazole oral therapy

Chromoblastomycosis / Chromomycosis Chromoblastomycosis is a chronic fungal disease of the skin and subcutaneous ssues, caused by a group of dema acaeous (black) fungi. It occurs worldwide, but most commonly in tropical and subtropical regions. Sri Lanka is a tropical country, in which the fungus has been isolated from soil (A apa u 1997). The infec on is usually introduced by trauma and is most o en diagnosed in men engaged in agriculture. Five causa ve fungi have been iden fied: Fonsecaea pedrosoi (most prevalent) Phialophora verrucosa Cladosporium carrionii Fonsecaea compacta Rhinocladiella aquaspersa They vary in their specific morphologic characteris cs of sporula on, which are evident on culture, but have only a single ssue form: pigmented sclero c bodies

commonly called copper pennies, which are pathognomonic of chromoblastomycosis. Treatments Chromoblastomycosis is notoriously difficult to treat, with no one form of treatment being uniformly successful. · Small lesions can be removed with wide and deep excision · Cryotherapy · Topical heat therapy · Itraconazole, 200–400 mg daily for a prolonged period, usually 8–12 months or longer · Terbinafine, fluconazole, 5-flurocytocine, saperconazole, and amphotericin B have also been used. Combina on of the above has been reported to be useful (Kumarasinghe 2000, Ranawaka et al 2009).

References 1. A apa u MC (1997). Chromoblastomycosis – clinical and mycological study of 71 cases from Sri Lanka. Mycopathologia 137 : 145. 2. Atukorala DN, Kumarasinghe SPW, Kumarasinghe MP et al.(1995). Cryotherapy in chromoblastomycosis. Sri Lanka J Dermatol 1: 7–8. 3. Kumarasinghe SPW, Kumarasinghe MP (2000). Itraconazole pulse therapy in chromoblastomycosis. Eur J Dermatol 10 :220–222. 4. Ranawaka RR, Amarasinghe N, Hewage D (2009). Chromoblastomycosis: combined treatment with pulsed itraconazole therapy and liquid nitrogen cryotherapy. Int J Dermatol. 48(4):397-400 5. Ungpakorn R, Reangchainam S (2006). Pulse itraconazole 400 mg daily in the treatment of chromoblastomycosis. Clin Exp Dermatol. 31: 245–247.

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Figure 3.1: A 59 year-old farmer was ini ally diagnosed with lupus vulgaris on histopathology, but did not respond to six months of an TB therapy (CAT1). Deep sec ons in a repeat skin biopsy showed occasional copper pennies that confirmed a diagnosis chromomycosis. Figure 3.2: A 48 year-old man who is a shoemaker with chromomycosis.

(a)

(b)

Figure 3.3: A 52-year-old male farmer with chromomycosis on the right ankle (a) at presenta on (b) a er 9 months of treatment with liquid nitrogen cryotherapy weekly and itraconazole monthly pulses.

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(4) a)

Impe go

b)

Staphylococcal scalded skin syndrome (SSSS)

c)

See chart below

Impetigo Impe go is a contagious, superficial pyogenic infec on of the skin. Two main clinical forms are recognized: non-bullous and bullous impe go. Impe go is most common in children. Causa ve organisms are Staphylococcus aureus Streptococcus pyogenes Non-bullous impe go may be caused by both S. aureus and streptococcal bacteria,

while bullous impe go is a superficial cutaneous infec on with S. aureus. Disease course and prognosis Impe go is usually self-limi ng and resolves within days to weeks with the appropriate use of topical cleansers and an bio cs. Spread to others in close contact with the index case is common and relapse is more frequently seen in individuals with underlying skin diseases and in staphylococcal carriers.

Management of impe go Wash skin, remove crust, and use disinfectants Localized skin involvement Apply topical an bio c twice daily to infected skin for one week

Impe go Extensive skin involvement, bullous disease and/or lymphadenopathy

Treat as for localized skin involvement plus systemic an bio cs (flucloxacillin, cloxacillin)

Reference Roderick J. Hay and Rachael Morris-Jones (2016). Bacterial Infec ons. In Rook's Text Book of Dermatology, 9th Edn, Wiley-Blackwell Science, UK, p 26.13

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Figure 4.1: Bullous impe go on the leg of a diabe c woman

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Figure 4.2: Non-bullous impe go on the face of a child

Figure 4.3: Non-bullous impe go on the legs of a child

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(5) a)

Tinea manuum (ringworm of the hand)

b)

Skin scrapings for fungal microscopy and fungal culture

c)

Terbinafine 250 daily for 2-4 weeks / Oral griseofulvin 500mg nocte for 3 months or longer. Relapse is common.

Fungal infections Figure 5.1: Tinea manuum Dermatophyte infec ons of the palm are o en quiet and chronic, and misdiag-nosed. Infec on spread to the dorsal surface is infrequent, if occurs more classic annular lesions may be seen. Causa ve organisms are Trichophyton rubrum (most common) Epidermophyton floccosum and Trichophyton interdigitale are involved in a small minority of cases.

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Clinical presenta ons Hyperkeratosis of the palms and fingers is the most common variety. Accentua on of the flexural creases is a characteris c feature. Unilateral scaling should always alert the clinician, concomitant onycho-mycosis may help. Differen al diagnosis Irritant contact derma s, psoriasis, pityriasis rubra pilaris, hand eczema, palmar keratoderma, syphilis and post streptococcal peeling.


Figure 5.2:

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Tinea corporis

Extensive nea corporis is mostly due to inappropriate treatment with topical steroids since nummular eczema is a common error. Treatment First line Oral terbinafine 250 mg/day 2–3 weeks. Second line Griseofulvin 1 g/day for 4 weeks. Con nue topical an fungal.

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Figure 5.3: Tinea imbricata Caused by Trichophyton concentricum, an anthropophilic dermatophyte found in southern Asia, the islands of the South Pacific and in Guatemala, Southern Mexico and Brazil, causes a dis nc ve infec on. It seems to affect mainly the na ve peoples of these areas. It occurs in both sexes and at all ages. The infec on begins as a scaling ring; centrifugal spread follows, but within the

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area of central clearing a second wave of scaling soon arises. The process is repeated to give numerous concentric rings and, as the natural history is normally prolonged, the whole body may become affected. Treatment Treatment failures may occur with griseofulvin. Both terbinafine and itraconazole are effec ve. ·

Oral terbinafine 250 mg/day 2–3 weeks

· Itraconazole 100 mg/day 2–4 weeks but may need prolonged treatments.


Figure 5.4: Tinea capi

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Present with few dull grey, broken-off hairs with a li le scaling. In all types, the cardinal fe a t u r e s a r e p a r a l h a i r l o s s w i t h inflamma on of some degree. If affected are school going careful inves ga on of the outbreak or epidemic is recommended. Causa ve organisms depend on the type of hair sha invasion; Ectothrix type – Microsporum spp; M. audouinii, M. canis. Fluorescence under the Wood's lamp. Endothrix type – Trichophyton spp; T. tonsurans, T. soudanense, T. violaceum.

En rely contained within and completely fill the hair sha . Hair thus affected is fragile, and breaks off close to the scalp surface. This type is non-fluorescent. Favus – T. schoenleinii. Affected hair is less damaged. Greenish grey fluorescence is present. Treatment ·

Terbinafine daily for 4 weeks

·

Itraconazole daily for 4-6 weeks (dose depend on the weight of the child)

·

Griseofulvin 6 weeks is given par cularly for Microsporum infec ons.

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Figure 5.5: Tinea nigra Asymptoma c, superficial fungal infec on caused by Hortaea werneckii.

The most dis nc ve feature is the brown or black colour. The palms are most commonly affected. Spontaneous clearance is unlikely.

More commonly found in tropical climates. This condi on is asymptoma c. The lesions are macular, sharply defined and not scaly.

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Treatment First line treatment is topical azole creams such as econazole and ketoconazole.


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(a) This army soldier was ini ally treated as sycosis barbae with poor clinical response to oral an bio cs.

(b) The lesion completely cured w i t h o u t l e av i n g a s c a r a e r treatment with oral griseofulvin 500mg nocte for 6 weeks.

Figure 5.6: Tinea barbae This is ringworm of the beard and moustache areas of the face with the invasion of coarse hairs. It is thus a disease of the adult male. Causa ve organisms T. verrucosum and T. mentagrophytes Clinical picture Highly inflammatory, pustular folliculi s, o en showing all the features of a kerion. Hairs of the beard or moustache regions are

surrounded by red inflammatory papules or pustules, usually with exuda on or crus ng. Differen al diagnosis – Sycosis barbae (S.aureus), acne, rosacea, pseudofolliculi s. Management Itraconazole or terbinafine, in combina on with topical therapy over a period of 4–6 weeks. Fairly long-term follow-up is recommended, and late recurrences can occur.

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Figure 5.7: Pityriasis versicolor Caused by Malassezia spp, lipophilic yeast; usually M. globosa and possibly M. sympodialis and M. furfur. Coloniza on by these species is dense in the scalp, the upper trunk and flexures – areas rich in sebaceous glands and their secre ons. In infants PV occur mainly periorbital. The colour of the scales may vary from pale ochre to medium brown. In untanned white skin, the affected areas are darker than normal, in the suntanned subject the abnormal skin is commonly paler, as it usually is in black people. Under the Wood's lamp, the scaly lesions may show pale yellow fluorescence. Depigmenta on thought to be due to the produc on of dicarboxylic acids produced by Malassezia species (e.g. azaleic acid) which cause compe ve inhibi on of tyrosinase

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and a direct cytotoxic effect on hyperac ve melanocytes. The explana on for the hyperpigmenta on seen in fair-skinned subjects remains obscure. Treatments

Topical azoles or terbinafine 1% cream twice daily for 2–3 weeks.

Ketoconazole or 2.5% selenium shampoo twice weekly for 2–3 weeks for wide body areas, and is applied to all the affected areas and le overnight.

Itraconazole 200 mg daily for 5 days, for extensive or recalcitrant cases.

Relapse is common. The residual depigmenta on may remain for many months without any scaling. Pa ents should be warned, as otherwise they will o en report treatment failure.


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Figure 5.8: Kerion Most severe pa ern of reac on; forms a painful, inflammatory mass. Lymphadenopathy is frequent. Caused by one of the zoophilic species, typically T. verrucosum or T. mentagrophytes. Infec vity from human to human is small. If treatment is delayed permanent hair loss from scarring is usual. The careful removal of crusts using wet compresses should not be neglected, and the possibility of coexis ng bacterial infec on should be considered.

Treatment Both terbinafine and griseofulvin are effec ve, but prolong treatments for 3-4 months may warrant un l completely cured without any sign of inflamma on. Domes c pets can o en be treated successfully and economically with griseofulvin.

Reference Roderick J. Hay and H. Ruth Ashbee (2016). Fungal Infec ons. In Rook's Text Book of Dermatology, 9th Edn, WileyBlackwell Science, UK, p 32.45

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(6) a) Candida infec on b) Frequent emersion of hands in water, poorly controlled diabetes mellitus, OCD (Obsessive compulsive disorder) c) Keep the affected area dry

Intertriginous candidosis Most cases of cutaneous candidosis occur in the skin folds or where occlusion from clothing or medical dressings produces abnormally moist condi ons. Any skin fold may be affected, especially in the obese subject. Satellite lesions, pustular or papular, are classic. Soreness, and itching, which may be intense, is usual. Topical steroids, prescribed for relief of itching, may modify the inflammatory signs and cause diagnos c confusion. Where the web spaces of the toes or fingers are affected, marked macera on with a thick, white, horny layer is usually prominent. Differen al diagnosis Tinea, seborrhoeic derma s, bacterial intertrigo, flexural psoriasis, Hailey–Hailey disease, flexural Darier disease.

Treatment Topical therapy (azole or polyene creams) usually con nued for about 2 weeks, but treatment may be required for longer periods. Treatment is likely to fail if a en on is not given to drying the affected area. In moist Candida intertrigo, potassium permanganate soaks are more effec ve. Treat concomitant bacteria; potassium permanganate is useful for this purpose. In finger or toe web infec ons, topical an fungal therapy, combined with the use of open footwear in the case of infec ons of the feet, is appropriate. Treatment of Candida onychomycosis Itraconazole 200mg b.i.d. for 1 week, monthly pulses; 2 pulses for finger nails, 3 pulses for toe nails.

References 1.

Ranawaka RR, de Silva N, Ragunathan RW (2012). Non-dermatophyte mold onychomycosis in Sri Lanka. Dermatol Online J. 15;18(1):7

2. Ranawaka RR, Nagahawa e A, Gunasekara TA, Weerakoon HS, S.H. Padmal de Silva (2015). Randomized, double blind, compara ve study on efficacy and safety of itraconazole pulse therapy and terbinafine pulse therapy on non-dermatophyte mold onychomycosis: a study with 90 pa ents. J Dermatolog Treat. 10:1-9. 3. Ranawaka RR, S.H. Padmal de Silva (2017). Factors influencing the clinical cure of non-dermatophyte and Candida onychomycosis. Int J Dermatol. 56, 202-208 4. Roderick J. Hay and H. Ruth Ashbee (2016). Fungal Infec ons. Rook's Text Book of Dermatology, 9th Edn, WileyBlackwell Science, UK, p 32.63

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Figure 6.1: Finger web candidosis in a housewife who frequently handles water.

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Figure 6.2: Toe web candidosis.

Figure 6.3: (a) Candida onychomycosis associated with paronychia; found in 29-32% onychomyco c pa ents presented to the hospital skin clinics in Sri Lanka. This is indis nguishable clinically from dermatophyte or non-dermatophyte mold onychomycosis. (b) Complete clinical cure a er itraconazole two pulses and topical an fungal lo ons for 12 months.

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Figure 6.4: Candida intertrigo (flexural candidosis) in submammary area in a 74 year-old obese woman. Typically erythema and a li le moist exuda on start deep in the fold. As the condi on develops, it spreads beyond the area of contact, usually developing the typical features of candidosis with a fringed, irregular edge and subcorneal pustules rupturing to give ny erosions.

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(7)

Becker naevus Becker naevus (or Becker melanosis) is a rela vely common hyperpigmented lesion with an incidence of around 0.25%. It is commoner in males than females. It is rarely congenital, with the majority of lesions appear in the first two decades, classically at puberty. It is frequently but not always hypertricho c, and is commonest on the upper trunk. Associa ons Becker naevus is not uncommonly asso ciated with extracutaneous abnormali es, then termed Becker naevus syndrome, which can involve underlying structures, namely aplasia or hypoplasia of the underlying breast ssue, or pectoralis major muscle (or some mes shoulder muscles) or lipoatrophy. Other extracutaneous associa ons described are ipsilateral limb growth disturbance, super numerary nipples and scoliosis.

Laser therapy Becker melanosis consists of dermal melanophages as well as epidermal hyperpigmenta on. Its response to Q-switched lasers or to flashlamps is unpredictable, par cularly if there is hypertrichosis, and repigmenta on may occur from the hair follicles. This has led some authors to suggest that abla ve treatment with an Er:YAG laser may be preferable. Despite early enthusiasm for frac onal abla ve lasers, treatment of Becker melanosis o en results in pos nflammatory hyperpigmenta on and poor pa ent sa sfac on.

Reference Veronica A. Kinsler and Neil J. Sebire (2016). Congenital Naevi and Other Developmental Abnormali es Affec ng th

the Skin. Rook's Text Book of Dermatology, 9 Edn, Wiley-Blackwell Science, UK, p 75.19 and 23.14

(8) a) Lip lick derma

s

b) Advice to get rid of the habit of lip licking c) Regular applica on of 1% hydrocor sone ointment

Lip lick dermatitis Moist or fissured eczema around the mouth is common in children with atopic eczema. Its persistence, and perhaps its origin, is a ributable to habits of lip licking, thumb sucking, dribbling or chapping. Contact sensi vity, for example to toothpaste ingredients, can occasionally be demonstrated. The regular applica on of 1% hydrocor sone ointment is usually most helpful.

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Cutaneous Larva Migrans The prime feature is that the lesion creeps or migrates, and that it is due to the presence of moving parasites in the skin.

This is exceedingly itchy. The disease is self-limi ng. Natural dura on of the disease vary depending on the species of larva; four weeks to many months.

Causa ve organisms These are all hookworms of various animals. Ancylostoma brasiliense. – Dog and cat hookworm is the commonest cause of creeping erup on in humans. Ancylostoma caninum. – Dog hookworm Ancylostoma ceylonicum. – Hookworm of dogs, cats and golden hamsters. Unicararia stenocephala. Bubostumum phlebotomum.

Treatment First line Ivermec n 200 μg/kg orally once daily for 1 - 2 days Second line Albendazole 400 mg orally for 3 days

Reference th

Christopher Downing and Stephen Tyring (2016). Parasi c Diseases. Rook's Text Book of Dermatology, 9 Edn, Wiley-Blackwell Science, UK, p 33.18

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Figure 9.1: A pregnant woman had this very itchy lesion on her abdominal skin for one week. Since she refused to take oral albendazole she was treated with local liquid nitrogen cryotherapy to the extending edge (head of the worm).

Figure 9.2: Same pa ent came a er 12 days with recurrent infec on (on le ). Note that the earlier lesion is cured. It is important to treat the domes c cat or dog with an helminthics to prevent recurrent infec ons.

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(10) a) Cutaneous horn b) Surgical excision is usually advised to obtain hitopathology and to rule out malignancy, commonly SCC

Cutaneous horn Cutaneous horns are hard conical projec- ons from the skin, made of compact kera n. They arise from benign, premalignant or malignant skin lesions. Cutaneous horns are more common in the older popula on with a peak incidence in those between 60 and 70 years. The lesions are most common on the exposed areas, par cularly the upper part of the face and the ears. In one large series these were commoner in females (Yu RC et al 1991). But in horns with pre-malignant or malignant ae ology, the lesions were commoner on light-exposed sites in older men. Disease course and prognosis There is an increased chance of finding pre-malignant or malignant change in the

base with increasing age. In long established lesions there may be budding from the basal layer, indica ng early development of a SCC. Just fewer than 40% have pre-malignant or malignant change, usually a SCC, at the base. Management A cutaneous horn is diagnosed by its clinical appearance. Histological examina on of the horn base is crucial to rule out malignancy, as there are no diagnos c clinical features that can defini vely dis nguish benign lesions from skin cancer. Surgical excision is usually advised to obtain pathology and rule out malignancy.

References

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1.

Girish Gupta , Vishal Madan and John T. Lear (2016). Squamous Cell Carcinoma and its Precursors. Rook's Text th Book of Dermatology, 9 Edn, Wiley-Blackwell Science, UK, p 142.11

2.

Yu RC , Pryce DW , MacFarlane AW , Stewart TW (1991). A histopathological study of 643 cutaneous horns Br J Dermatol 124 : 449 – 52 .


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Figure 10.1: An 80 year-old woman with a cutaneous horn and seborrhoeic keratoses.

Figure 10.2: A 66 year-old woman with cutaneous horn on the dorsum of le hand. These are commoner in females as in our three cases. None of them showed malignant changes.

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(11) Scabies specific. They include excoria ons, and impe giniza on. ·

·

·

Caused by a mite, Sarcoptes scabiei var. hominis. Itching is the most obvious manifesta on usually sparing the face in adults. Itching worst at night and when the pa ent is warm. Symptoms start 3–4 weeks a er the infec on is acquired. Diagnosis The typical history of pruritus with nocturnal exacerba ons, the presence of contact cases within the family and the distribu on of the erup on of inflammatory papules, should suggest the diagnosis. The presence of genital lesions in men or breast nodules in women is strongly sugges ve. Absolute confirma on can only be made by the discovery of burrows and/or microscopic examina on. Typical loca ons of lesions are the finger webs, the flexor surfaces of the wrists, the elbows, the axillae, the bu ocks, genitalia and the breasts of women. Nodules are intensely itchy, and may persist for weeks or months a er the scabies has been effec vely treated. Itching may persist several weeks a er scabies is completely cured. The persistence of itching a er 4 weeks should be reinves gated. Secondary lesions are non

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Scabies in infants and young children more extensive distribu on of burrows, vesicular and vesiculopustular lesions on the hands and feet are frequent, extensive eczema za on is o en present, and there may be mul ple crusted nodules on the trunk and limbs. Elderly – burrows commonly occur on the palms and soles, and may be very numerous. Truncal papulosquamous lesions, o en surmounted by burrows, are common. Secondary eczema za on is o en troublesome. Crusted scabies (Norwegian scabies) Large warty crusts form on the hands and feet, and the palms and soles may be irregularly thickened and fissured. In common scabies, there are few mites, probably because scratching destroys the burrows. Crusted scabies occurs in people with an inadequate immune response to the mite allowing them to mul ply, mentally retarded, suffer from demen a or Down syndrome.

Atypical forms of scabies are very difficult to diagnose. · Scabies of the scalp – Scabies may accompany or simulate seborrhoeic derma s or dermatomyosi s on the scalp; infants, children, the elderly, pa ents with AIDS and pa ents with crusted scabies may be affected. · Nodular scabies – A few violaceous, pruri c nodules are o en localized on the groin, axillae and male genitalia (Figure above); they represent a hypersensi vity reac on to mite an -gens and persist weeks or months a er treatment. Reference: Gen ane Monsel, Pascal Delaunay and Olivier Chosidow (2016). Arthropods. Rook's Text th Book of Dermatology, 9 Edn, Wiley-Blackwell Science, UK, p 34-39.


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(12) a) Fish tank granuloma b) Mycobacterium marinum c) Sporotrichoid spread

Fish tank granuloma (Mycobacterium marinum infec on/ Swimming pool granuloma)

Differen al diagnosis Leishmaniasis and sporotrichosis in endemic areas. Other atypical mycobacterial infec ons (for example, M. kansasii, M. chelonae and M. gordonae) all of which may spread in a sporotrichoid manner. Diagnosis A history of contact with water, fish tanks, aquariums, etc., combined with granulomatous histology, is sugges ve of the diagnosis. A posi ve culture can be obtained in some 70–80% of cases.

Mycobacterium marinum causes disease in many fish species and human infec on follows contact with fish or contaminated water. The natural habitat of M. marinum is fresh or salt water, par cularly enclosures of water that are not o en replenished, such as swimming pools and aquariums. Although a history of trauma cannot always be elicited this is only pathogenic on abraded skin. Most infec ons are acquired while cleaning the tanks.

Treatments M. marinum is a naturally drug-resistant species.

Average incuba on period is 2–3 weeks (can be as long as 9 months). Lesions are o en mul ple. In the sporotrichoid form, which occurs in approximately 20% of cases, nodules may extend along the line of lympha c vessels.

Treatment failure is more usually related to the involvement of deeper structures, delay in diagnosis and inappropriately administered intralesional steroids. Deep M. marinum infec on involving the hand can be aggressive and may result in permanent disability.

Deeper infec ons may be complicated by tenosynovi s, osteomyeli s, bursi s and sep c arthri s. Immunocompromised pa ents may develop disseminated lesions.

Clarithromycin / Azithromycin and Ethambutol for 1–2 months a er the resolu on of symptoms (typically 3–4 months in total) (Rifampin should be added in cases of osteomyeli s or other deep structure infec on)

Reference Victoria M. Yates and Stephen L. Walker (2016). Mycobacterial Infec ons. Rook's Text Book of th Dermatology, 9 Edn, Wiley-Blackwell Science, UK, p 27-33.

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(13) a) Oral submucous fibrosis (OSF)/ vi ligo on lips b) Examine the oral cavity, In OSF the oral mucosa is white and firm, restricted opening of the mouth. c) Beetle chewing d) Biopsy from the oral mucosa

Oral submucous fibrosis Oral submucous fibrosis (OSF) is found virtually exclusively in persons from the Indian subcon nent; most of those affected chew Areca nut with tobacco, betel leaf and lime. It appears to be caused by exposure to cons tuents of the Areca nut. OSF develops insidiously, o en ini ally presen ng with oral dysaesthesia (burning sensa on) and a non-specific vesicular stoma s. This appears to be restricted to the mouth, although many pa ents are also anaemic. The affected site becomes white and firm, with severely restricted opening of the mouth. Histopathology There is a subepithelial chronic inflammatory reac on with fibrosis extending to the

submucosa and muscle. Epithelial changes range from atrophy to keratosis and there may be dysplasia. Prognosis OSF predispose to the development of oral carcinoma, which occurs in 2–10% of pa ents over a period of 10 years. Management is difficult. Intralesional cor costeroids and jaw exercises may be useful in the early stages, but surgery may be needed to relieve the fibrosis. Reference Crispian Scully (2016). Dermatoses of the Oral Cavity th and Lips. Rook's Text Book of Dermatology, 9 Edn, Wiley-Blackwell Science, UK, p 110.56

Figure 13.1: A 35 year-old man complained of depigmenta on of lips for 6 months. Protruding the tongue was difficult and ght. Glossi s and angular stoma s is shown in this picture. He gave a history of frequent beetle chewing.

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Figure 13.2: Chronic beetle chewer (evident from her discoloured decayed teeth) presented with non-healing ulcer on the lower lip. On examina on glossi s, angular stoma s and untreated submucous fibrosis noted. This is the maximum she could open her mouth, and protrude her tongue. The ulcer on the lip was confirmed squamous cell carcinoma by histopathology.

Figure 13.3: A 66 year-old woman who is addicted to beetle chewing complained of burning sensa on in the mouth, lips and the tongue. Above shown was the maximum she could open her mouth and protrude her tongue out.

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(14) a) Acanthosis nigricans (benign type) b) Obesity, skin tags in neck, hirsui sm c) Tests for insulin resistance (Serum Insulin)

Acanthosis nigricans Acanthosis nigricans (AN) is a dermatosis that manifests as asymptoma c and symmetrical darkening affec ng the skin of intertriginous areas, in par cular the axillae, groins, submammary folds and neck. The skin in those regions is thickened, has a velvety texture, and may be studded by skin tags. AN is more common in pa ents with darker skins. Associa ons Divided into two important categories, benign and malignant. Benign acanthosis nigricans is o en associated with obesity or insulin resistance, and is common and usually mild, (previously called pseudo-AN), and can regress with weight loss. It has been documented in up to 20% of adults and 7% of children, mainly in the teenage years; virtually all childhood cases are of the benign type. M a l i g n a n c y- a s s o c i a t e d a c a n t h o s i s nigricans is much less common. It may have a rapid onset and progression to produce symmetrical, hyperpigmented, rugose,

velvety plaques. The axillae and other flexures are par cularly affected, along with the areolar area and nape of the neck and, less commonly, mucosal surfaces. Malignancy to be suspected if, Tripe palms If progressive and associated with weight loss Generalized pruritus Commonest site of underlying neoplasm is the gastrointes nal tract (70–90%); gastric adenocarcinoma is the most frequent. Many syndromes have been associated with AN; they usually involve the endocrine system or accompany autoimmune disorders. Assessment In adult-onset AN, pa ents should be screened for underlying endocrinopathy or malignancy. A sensi ve test for insulin resistance is serum insulin, the levels of which may be elevated before the onset of diabetes or eleva on of glycosylated haemoglobin levels.

References

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1.

Lennart Emtestam and Karin Sartorius (2016). Cutaneous Markers of Internal Malignancy. Rook's Text Book of th Dermatology, 9 Edn, Wiley-Blackwell Science, UK, p 147.14

2.

Anthony C. Chu and Fernanda Teixeira (2016). Acquired Disorders of Epidermal Kera niza on. Rook's Text th Book of Dermatology, 9 Edn, Wiley-Blackwell Science, UK, p 87.


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Figure 14.1: Extensive acanthosis nigricans involving all the flexures are not uncommon in obese men. There are skin tags in his axilla too.

Figure 14.2: Facial acanthosis is not uncommon in obese men and women. Note this woman having acanthosis nigricans on her face and neck.

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(15) a) This is allergic contact derma s to underwear (brazier) b) Examina on with proper exposure. Otherwise the features of contact derma s may obscure and the diagnosis of eczema is made. c) Avoid allergens. e.g. in this case it could be either fabric material or the fabric dye. Patch tests can be performed to iden fy it specifically.

Allergic contact dermatitis Allergic contact derma s is an eczematous reac on that occurs as an immunological response following exposure to a substance to which the immune system has previously been sensi zed.

Management Avoiding the causa ve substance or the use of appropriate personal protec ve equip ment (e.g. gloves made of an appropriate material).

The diagnosis of allergic contact derma s can only be confirmed by patch tes ng and should always be used to exclude contact allergy as a complica ng factor in stubborn cases of eczematous diseases, as well as cases where allergic contact derma s is suspected from the pa ern or distribu on of the eczema.

Desensi za on for the majority of relevant allergens is not available. Reference Mark Wilkinson and David Orton (2016). Allergic C o n t a c t D e r m a s . R o o k ' s Te x t B o o k o f th Dermatology, 9 Edn, Wiley-Blackwell Science, UK, p 128.13

Figure 15.1: Commode derma s; allergic contact derma to the commode, commonly seen in young children.

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Figure 15.2: Allergic contact derma

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s to nickel in the waist belt.

Figure 15.3: Allergic contact derma

s to rubber slippers.

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Figure 15.4: A professional driver with allergic contact derma covering of the steering wheel.

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s to the rubber

Figure 15.5: Allergic contact derma s to “Wathusudda flower” affec ng only first three fingers on both hands in a frequent Buddhist worshipper.

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(16) a) Halo naevus b) Vi ligo, rarely melanoma surrounded by a halo

Halo naevus The development of a halo of hypomelanosis around a central cutaneous tumour. This tumour is usually a benign melanocy c naevus but may be a neuroid naevus, blue naevus, neurofibroma, or primary or secondary malignant melanoma. Most halo naevi are compound naevi, although a junc onal or dermal naevoid pa ern is also possible. Both congenital and acquired naevi can be affected. Disease course and prognosis The naevus tends to fla en and may disappear completely. The depigmented

areas o en persist, but may pigment a er many years. Complica ons and co-morbidi es Halo naevi can be present with or without associated vi ligo lesions. Management Normally none is required. The usual diagnos c criteria must be applied if there is any possibility that the central tumour is malignant. It should be remembered that a halo around a benign naevus is rela vely common, whereas malignant melanoma is rare, and a melanoma surrounded by a halo is extremely rare.

Reference Nanja van Geel and Reinhart Speeckaert (2016). Acquired Pigmentory Disorders. Rook's Text Book of Dermatology, th 9 Edn, Wiley-Blackwell Science, UK, p 88.40.

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(17) a) Tuberculoid leprosy with type I reac on/ lupus vulgaris/ cutaneous sarcoidosis b) Skin biopsy and smear from the plaque for acid fast bacilli c) She can con nue breast feeding during her an leprosy drug treatments. Child can get clofazimine pigmenta on if the mother is on mul bacillary therapy; i.e. daily dapsone, daily clofazimine and monthly rifampicin. This pigmenta on disappear spontaneously 68 months a er cessa on of therapy. Drugs should be con nued during pregnancy and breast feeding.

Leprosy

Fig 17.1: A 10 year-old girl came with six hypopigmented patches. Four patches are visible in this photograph on her face (n=3) and right forearm (n=1) (Mul bacillary leprosy).

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Fig 17.2: A 45 year-old man complained of change of his facial appearance over last six months (Lepromatous leprosy / early leonine facies).

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Figure 17.3: These pa ents presented with recurrent ulcers on hands and feet. On direct inquiry peripheral numbness revealed (Lepromatous leprosy).

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Figure 17.4: This young man presented to the neurologist with bilateral claw hand deformity. He did not have skin patches (Neural leprosy).

Figure 17.5: A 35 year-old man complained of non itchy, mildly tender plaque on his le cheek for five days. His le greater auricular nerve was palpable, cord like and was tender (Tuberculoid leprosy with type I reac on).

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Figure 17.6: A 79 year-old man with lepromatous leprosy with mixed Type I and Type II reac ons.

Figure 17.7: Erythema nodosum leprosum (ENL) lesions (Type II reac on).

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(18) a) A pa ent with generalized vi ligo showing sparing of slipper contact area (reverse Kobner phenomena)

Vitiligo Vi ligo is a common form of localized depigmenta on. It is an acquired condi on resul ng from the progressive loss of melanocytes. Associated diseases Amongst autoimmune diseases, the strongest associa on is with thyroid disease. The associa on between vi ligo and halo n a e v i i s we l l e sta b l i s h e d . A re a s o f depigmenta on some mes develop in pa ents with melanoma. Gene cs Approximately 30% of pa ents have a posi ve family history.

applica ons are recommended, ini ally for 6 months. Second line Systemic psoralen photochemotherapy (PUVA) UVB therapy Irradia on will be stopped if no repigmenta on occurs within the first 3 months of treatment. Third line Gra ing techniques for stable vi ligo (e.g. segmental vi ligo). This is to transplant autologous melanocytes from a normal pigmented area to the affected depigmented skin.

Management First line Once-daily applica on of potent topical cor costeroid prepara ons – preferable to use an intermi ent regimen (e.g. 15 days per month for 6 months) to avoid local side effects (skin atrophy, telangiectasia, striae, hypertrichosis and acneform erup ons)

Use of topical calcineurin inhibitors (pimecrolimus, tacrolimus) has been reported to be successful, mainly for lesions on the face and neck: twice-daily

This can be either ssue gra s (full-thickness punch gra s, split-thickness gra s, suc on blister gra s) or cellular gra s (cultured melanocytes, cultured epithelial sheet gra s and non-cultured epidermal cellular gra s).

Depigmen ng treatment with extensive vi ligo and only a few residual areas of pigmenta on, skin bleaching with laser therapy (e.g. Q-switched alexandrite 755 nm, Q-switched ruby 694 nm), cryotherapy or creams (e.g.20% mono benzylether of hydroquinone), may be used.

Reference Nanja van Geel and Reinhart Speeckaert (2016). Acquired Pigmentory Disorders. Rook's Text Book of Dermatology, th 9 Edn, Wiley-Blackwell Science, UK, p 88.34

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Figure 18.1: Vi ligo appearing only on the area of rubber slipper contact (Koebner phenomena).

Figure 18.2: Localized vi ligo on scalp may cause localized area of white hair resembling piebaldism.

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Figure 18.3: This vi liginous patch at the natal cle is due to post inflammatory hypopigmenta on following intralesional steroid injec ons to the site.

Figure 18.4: This vi liginous area along the hair line is following hair dye allergy.

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Figure 18.5: Segmental vi ligo: typically unilateral maculae in a segmental/ band-shaped distribu on.

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Pigmentary mosaicm Gene cally determined varia on of skin pigmenta on. Present as streaks and whorls of hypo or hyperpigmenta on following Blaschko's lines with midline demarca on. May also manifest as patches, flag-like, leaf-like (phylloid) or chequerboard shapes, or as patchy varia on without midline demarca on.

Management Infants with pigmentary mosaicism should be thoroughly assessed with par cular a en- on to development, the internal organs and skeletal and ophthalmological abnormali es. Parents of the child to be educated that this problem is incurable and will persist for life.

Reference th

Alan D. Irvine1 and Jemima E. Mellerio (2016). Chromosomal Disorders. Rook's Text Book of Dermatology, 9 Edn, Wiley-Blackwell Science, UK, p 117.12

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(20) a) Excision of this growth with a wider margin. Any growth arising on a long standing scar or ulcer should consider as SCC unless proven otherwise.

Squamous cell carcinoma Squamous cell carcinoma (SCC) is the second commonest skin cancer a er BCC. The incidence of SCC increases with age. Squamous cell carcinoma is predominately a disease of white popula ons and is especially prevalent in this group in areas of high ambient sun exposure. Pa ents with Fitzpatrick skin types I and II, par cularly

those with freckling and high UVR exposure are most at risk. Factors implicated in the pathogenesis of cutaneous malignancy in Africans and African Americans include trauma, albinism, burn scars, ionizing radia on, chronic inflamma on and chronic discoid lupus erythematosus.

Reference Girish Gupta, Vishal Madan and John T. Lear (2016). Squamous Cell Carcinoma and its Precursors. Rook's Text Book th of Dermatology, 9 Edn, Wiley-Blackwell Science UK, p 142.29

Figure 20.1: A 44 year-old woman with oozing eczematous growth on le middle finger, which was diagnosed SCC by histopathology. Differen al diagnosis was acral malignant melanoma which is common in pigmented skin.

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Figure 20.2: A 64 year-old man with warty growth on penile skin for three months; confirmed SCC by histopathology

Figure 20.3: A 74 year-old woman came with this non healing small 1cm x 1.5 cm diameter ulcer on her le cheek for six months; confirmed SCC by histopathology.

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(21) a) BCC b) See text c) Liquid nitrogen cryotherapy to seborrhoeic keratoses, electrocautery or TCA (trichloro ace c acid) applica on to DPN

Basal cell carcinoma Approximately 80% of all basal cell carcinoma (BCC) occur on the head and neck, and clinical diagnosis is rela vely straigh orward. Early BCCs are usually small, t r a n s l u c e n t o r p e a r l y, w i t h r a i s e d telangiecta c edges. More advanced lesions can present as classical rodent ulcer with an indurated edge and an ulcerated centre.

1. Topical Imiquimod

Clinical variants

2. Photodynamic Therapy

1.

3. Excision with margin (4-5mm surgical margin)

2.

Nodular BCC (Figure 22.1) is the commonest subtype of BCC and usually presents on the head and neck. Pigmented as well as nodular BCC may cause diagnos c confusion with melanoma. Superficial BCC (Figure 22.2) are less common and predominantly present on the trunk. Superficial BCCs are o en pigmented and can some mes be difficult to differen ate from psoriasis, discoid eczema or Bowen disease.

3.

Morphoeic BCC – have ill-defined borders, can be difficult to diagnose clinically and o en present late. Dense fibrosis of the stroma produces a thickened plaque rather than a tumour.

4.

Fibroepithelial basal cell carcinoma (premalignant fibroepithelial tumour) is a benign-appearing pedunculated pink premalignant tumour that may resemble a skin tag.

5.

Advanced and metasta c basal cell carcinomas are a manifesta on of prolonged neglect.

6. Ulcerated basal cell carcinomas may start as a small macule or papule but with expansion of the thread-like margins, the a enuated surface ulcerates.

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Management Both tumour (clinical and histological nature, size and site) and pa ent factors determine the choice of treatment of BCC. Other factors dicta ng choice of treatment include local experience and availability of treatments, which may indirectly depend upon the cost.

4. Mohs micrographic surgery 5. Cure age and electrodesicca on 6. Cryosurgery – The applica on of liquid nitrogen 7. Superficial and electron beam radiotherapy 8. Carbon dioxide laser Naevoid basal cell carcinoma syndrome (NBCCS) – An autosomal dominant familial cancer syndrome in which affected individuals are predisposed to the development of mul ple BCCs at an early age and a variable combina on of other phenotypic abnormali es including a highly charact-eris c facies (with large forehead), bifid or otherwise misshapen ribs, vertebral and other skeletal anomalies, pits of the skin of the palms and soles, dysgenesis of the corpus callosum, calcifica on of the falx cerebri (at an earlier age than is seen in non-affected individuals) and macrocephaly.


Follicular atrophoderma and basal cell carcinoma syndrome (Bazex) – A rare genodermatosis that predisposes affected individuals to mul ple BCCs. Addi onal

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clinical features that allow dis nc on from NBCCS include follicular atrophoderma, hypotrichosis and hypohidrosis. X-linked dominant disorder. Only females are affected.

Figure 21.1: A 44 year-old man came with numerous (more than 30) pigmented papules and nodules on his face, trunk and limbs. Four lesions were excised and found BCC in one and seborrhoeic keratoses in other three. He did not have other features of naevoid basal cell carcinoma syndrome (NBCCS). Pa ent was referred to the oncologist for opinion on further management.

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Fig 21.2: A 74 year-old man with oculocutaneous albinism had mul ple BCCs (nodular and superficial variants) and Bowen's disease on the trunk and both breasts. The reduc on of the amount of melanin is responsible for an increased sensi vity to UV radia on, loss of natural sun protec on, and for predisposi on to skin cancers. In this pa ent a few lesions were confirmed by excision, and since he had mul ple lesions and these were recurring for last fi een years, other suspicious lesions were treated with liquid nitrogen cryotherapy. Reference Vishal Madan and John T. Lear (2016). Basal Cell Carcinoma. Rook's Text Book of Dermatology, 9th Edn, WileyBlackwell Science, UK, p 141.9

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Lichen striatus Self-limi ng and asymptoma c inflammatory dermatosis characterized by pink or red papules in a linear distribu on that develop in the lines of Blaschko. These usually occur as isolated lesions on the limbs in children aged 5–15 years. Females are affected approximately two to three mes as frequently as males. Disease course and prognosis The onset is usually sudden. Frequently, there are no symptoms, but pruritus may occasionally occur and is more common in adults. The course is variable. The area affected typically reaches its maximum extent within 2–3 weeks, but gradual extension can con nue for several months. Spontaneous resolu on can be expected within 6–12 months in most cases, but some lesions may persist for over a year. Resolu on may be followed by hypopig-menta on or rarely hyperpigmenta on.

Differen al diagnosis Linear psoriasis, linear Darier disease, linear lichen planus, linear porokeratosis and inflammatory linear verrucous epidermal naevus (ILVEN). During hypopigmented stage linear vi ligo or nevoid hypomelanosis. Management First line Observa on and reassurance Topical cor costeroids in pa ents with troublesome itch (usually adults) Second line Topical tacrolimus Topical pimecrolimus

Reference Vincent Piguet, Stephen M. Breathnach and Laurence Le Cleach (2016). Lichen Planus and Lichenoid Disorders. th Rook's Text Book of Dermatology, 9 Edn, Wiley-Blackwell Science, UK, p 37.18

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Erythrasma -

Chronic localized superficial infec on of the skin caused by Corynebacterium minussimum. It occurs in the groins, axillae and the intergluteal and submammary flexures. The patches are of irregular shape and sharply marginated, at first red, but later becoming brown. New lesions are smooth, but older lesions tend to be finely creased or obviously scaly. In temperate climates most lesions are symptomless, but in the tropics irrita on of the lesions in the par cularly groins may lead to scratching and lichenifica on. A warm humid climate is a predisposing factor.

Inves ga ons Wood's light examina on shows pink fluorescence. Coral-red fluorescence is a ributable to coproporphyrin III and strongly suggests erythrasma, but not necessarily indicate ac ve infec on. Management Without treatment the condi on tends to persist indefinitely, although there may be spontaneous fluctua ons in severity. First line Erythrasma responds well to most topically applied azole an fungal agents, clotrimazole and miconazole. The dura on of therapy varies, but 2 weeks is usually sufficient. For more extensive lesions, erythromycin is probably the most effec ve.

Differen al diagnosis 1. Pityriasis versicolor is most commonly confused with erythrasma, but it occurs predominantly on the upper trunk, and the individual lesions are small and are not erythematous. 2. Tinea cruris – lack of inflamma on, complete absence of vesicula on and absence of satellite lesions point against nea. 3. It is difficult to differen ate erythrasma of the toe cle s from nea pedis or Candida infec on.

Relapse is a problem in some pa ents. In these pa ents usual approach is to give long-term an sep cs, such as povidone –iodine, and to use drying agents, such as powders, in the affected areas. Second line Photodynamic therapy

Reference th

Roderick J. Hay and Rachael Morris-Jones (2016). Bacterial Infec ons. Rook's Text Book of Dermatology, 9 Edn, Wiley-Blackwell Science, UK, p 26.39

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Figure 23.1: Co-exis ng acanthosis nigricans and erythrasma are not uncommon in obese men. This man has acanthosis nigricans in flexures and on the face.

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(24) a) Chronic ac nic derma s b) Photoprotec on and avoidance of sunlight exposure

Photodermatoses Can be broadly categorized as Idiopathic (immunological): Polymorphic light erup on (PLE) Juvenile spring erup on (JSE) Ac nic prurigo (AP) Chronic ac nic derma s (CAD) Solar ur caria (SU) Hydroa vacciniforme (HV) Genophotodermatoses Metabolic Drug- or chemical-induced photosensi vity Endogenous – porphyrias Exogenous – systemic or topical drug/chemical photosensi vity Photoaggravated skin diseases

Chronic ac nic derma

Management First line Very potent/potent topical cor costeroids Topical tacrolimus or pimecrolimus can be effec ve. PUVA, UVB phototherapy Second line In-pa ent nursing behind visible- and UVabsorbing window film may be required.

s (CAD)

CAD is a persistent or recurring derma s predominantly affec ng photo-exposed sites. There is evidence of photosensi vity. Differen al diagnosis a) Airborne contact derma s – typically involves the upper eyelids and under the nose and chin, while the back of neck is spared. b) Photoaggravated atopic or seborrhoeic eczema – may be impossible to dis nguish from CAD on clinical grounds. c) Drug-induced photosensi vity. d) Cutaneous T–cell lymphoma, especially if there is erythroderma, must be considered.

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Complica ons and co-morbidi es Most pa ents have pre-exis ng or concurrent eczema: endogenous, atopic, and seborrhoeic or contact allergic. Sunscreen allergy/photoallergy may occur.

Third line Azathioprine 150 mg/day, can be used as a steroid-sparing agent. Hydroxychloroquine, ciclosporin, mycophenolate mofe l, hydroxycarbamide, etre nate, danazol, thioguanine, topical nitrogen mustard, thalidomide, infliximab and INF-α, have been reported to be effec ve but only in small case series and case reports. The avoidance of combined photo (chemo) therapy and systemic immunosuppressants, par cularly ciclosporin, is advised due to photocarcinogenic risk.


Figure 24.1: Chronic ac nic derma areas.

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s: lichenified skin showing clear demarca on to sun exposed

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Figure 24.2: Polymorphic light erup on: Itchy depigmented rash on the face is common in school children. Secondary 'eczema za on' develops par cularly in atopic pa ents if itching persists.

Figure 24.3: Polymorphic light erup on: Generalized non-itchy depigmented rash on face and trunk on sun exposed areas in a pre-school child.

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Polymorphic light erup on (PLE)

Solar ur caria

(PLE) is a recurrent, delayed-onset, abnormal reac on to sunlight (or ar ficial UVR source) that resolves without scarring. It is common and has a wide range of severity but can markedly affect quality of life. The diagnosis is usually straigh orward and based on history. PLE is much commoner in females.

Immediate development of ur caria following exposure to UVA, visible and less commonly UVB radia on.

Management of PLE First line · Sun avoidance and protec ve measures are sufficient for most mild/moderately affected people · Broad-spectrum high SPF sunscreens should be used and applied correctly (thickly, evenly and frequently) · Topical or systemic cor costeroid therapy Second line Prophylac c phototherapy/ photo chemotherapy is the main second line therapy used. PUVA is more effec ve than broad-band UVB. Narrow-band (TL-01) UVB is as effec ve as PUVA. Courses given in the spring serve to 'harden' the skin (by tanning and epidermal thickening and/or effects on immune responses) and are beneficial in most pa ents. Third line Long-term immunosuppressive drugs, such as azathioprine and ciclosporin have been used for refractory cases. Long-term i m m u n o s u p p re s s i ve d r u g s , s u c h a s azathioprine and ciclosporin have been used for refractory cases.

Exogenous photoseni sers Systemic l Diure cs: thiazides, furosemide, nalidixic acid l An bio cs: fluoroquinolones, tetracyclines , sulphonamides, l non-steroidal an inflammatory drugs, l an psycho cs: phenothiazines (chlorpromazine), cardiology: amiodarone, l calcium antagonists, ACE inhibitors, sta ns, l Hypoglycaemics: sulphonylureas, An fungals: voriconazole, itraconazole, ketoconazole, re noids, psoralens, quinine, l hydroxychloroquine, BRAF inhibitors, l pirfenidone, l An hepa s C drugs, l leflunomide, l venlafaxine, escitalopram, l Celecoxib, l Exogenous porphyrins for photodynamic therapy, Ima nib, l Aazathioprine, l fibrates, pyridoxine B6. Topical l Psoralens (phototoxic), polycyclic aroma c hydrocarbons (phototoxic), dyes (phototoxic) l Phenothiazines (chlorproethazine) (phototoxic and photoallergic), l Halogenated salicylanilides (mainly photoallergic), l fragrances (phototoxic and photoallergic), l sunscreens (phototoxic and photoallergic), l Non-steroidal an inflammatory drugs (phototoxic and photoallergic)

Reference Sally Ibbotson and Robert Dawe (2016). Cutaneous Photosensi vity Diseases. Rook's Text Book of Dermatology, 9th Edn, Wiley-Blackwell Science, UK, p 127.2, 127.13

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(25) a) Acroderma s enteropathica b) Zinc supplements c) Con nue zinc (Zn) for a long period under observa on of a dermatologist or a pediatrician.

Acrodermatitis Enteropathica This is an autosomal recessive disorder affec ng the intes nal absorp on of zinc. The resul ng zinc deficiency leads to derma s, alopecia and diarrhoea. This is very rare (approximately 1: 500 000).

of the skin, for example with Candida albicans. Wound healing is poor and many pa ents have diarrhoea and growth faltering. Without treatment, the condi on can be fatal but some pa ents survive into adulthood.

Pathophysiology Acroderma s enteropathica is caused by defects in ZIP4, the main intes nal zinc transporter. Zinc is a co-factor for many enzymes. The skin, intes ne and immune system are most severely affected because of their rapid cell turnover.

Inves ga ons The serum zinc concentra on is usually low b u t ca n b e n o r m a l . D e c re a s e d z i n c absorp on can be demonstrated using radioisotopes. But it is easier to undertake a trial of zinc therapy: pa ents respond within a week.

Clinical features Pa ents present with apathy or irritability and a rash around the mouth and anus and on the hands and feet. Symptoms start a er weaning in breas ed babies and at 4–10 weeks of age if they are formula-fed. Erythema progresses to vesicles, bullae, pustules, desquama on and crus ng. There is alopecia and frequently blephari s, conjunc vi s and photophobia. Infec ons are common, including secondary infec ons

Management Pa ents respond to oral zinc sulphate within a few days. The normal dose is 150–400 mg/day in childhood; a lower dose may suffice a er puberty. A 400–500 mg/day is needed during pregnancy. Monitoring for copper deficiency should be undertaken.

Reference th

Andrew Morris (2016). Inherited Metabolic Diseases. Rook's Text Book of Dermatology, 9 Edn, Wiley-Blackwell Science, UK, p 81.17

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25.1: A six months old baby before Zn supplements.

25.2: Four days a er Zn supplements. Response to the trial of Zn therapy is very drama c and is diagnos c.

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Clinical Dermatology in Pigmented Skin Volume I

WITH OVER 125 COLOUR ILLUSTRATIONS This book illustrates unusual presentaons of common skin diseases in tropics. Over 30 diseases are discussed and the answers are given with a brief descripon of the disease and further illustraons and descripon on the related dermatoses. This book has been wri en by a clinician for clinicians, to provide a clear and easy guide to idenfy common skin diseases prevalent in tropics.

Ranthilaka R. Ranawaka MBBS (Colombo) MD (Dermatology) Consultant Dermatologist General Hospital Kalutara Sri Lanka.

ISBN 978-955-38441-0-1