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INSIDE

General approach

Vitiligo

Infective causes

Other acquired disorders

Genetic and congenital disorders

the authors

Dr Deepani Rathnayake consultant dermatologist, Base Hospital Dambulla, Sri Lanka.

Background

DISORDERS of pigmentation are Disorders of Professor Rod Sinclair a common presentation in derma- director and head, dermatology, tology and general practice. Part 1 Epworth Hospital, Melbourne, of this update on disorders of pig- Victoria. mentation outlined the physiology of skin pigmentation and the path- pigmentation ological mechanisms that lead to these disorders. It then discussed the general approach to pigmentary dis- orders and focused on the diagnosis — Part 2: and management of hyperpigmen- tary disorders. , like hyper- pigmentation, can lead to signifi- cant psychosocial problems. It can Hypopigmentation even be a reason for social rejec- tion. This is especially pertinent in the cosmetic management of the This is the second of a two-part series on disorders of pigmentation. Part 2 covers hypopigmentary hypopigmented lesions that can be disorders in detail. significantly disfiguring on the face and other exposed skin. Acquired hypopigmentation may be associ- ated with an underlying systemic disorder that may be treatable. The search and treatment for underlying Copyright © 2014 conditions are just as important as Australian Doctor All rights reserved. No part of this the management of the presenting publication may be reproduced, cosmetic complaint. distributed, or transmitted in any This article discusses the general form or by any means without approach to hypopigmented skin the prior written permission of the publisher. lesions and then specific hypopig- For permission requests, email: mentary conditions in more detail. [email protected] cont’d next page

www.australiandoctor.com.au 18 April 2014 | Australian Doctor | 23 How To Treat – Disorders of pigmentation— Part 2: Hypopigmentation

General approach HYPOPIGMENTARY disorders The use of a Figure 1: may be due to both genetic and Hypopigmentation acquired causes. The pathogenic Wood’s lamp can in a patient with mechanisms by which hypopig- considerably improve systemic sclerosis mentation occurs can be broadly on the extensor divided into two processes: the diagnosis of surface of the right • Reduced or absent ; hypopigmentary elbow. or • Reduced number of melano- lesions, especially in somes and in the skin patients with lighter (table 1). skin colour. Diagnosis Most hypopigmentary disorders can be diagnosed with a detailed history and examination. A hypo- pigmented lesion present at birth may be a naevus or an ash-leaf macule. A history of a preceding Wood’s lamp examination on skin rash favours the diagnosis of Table 1: Pathogenic mechanism in hypopigmentary disorders hypopigmented lesions are shown post-inflammatory hypopigmenta- Disease Defect in the table below left. tion. The presence of anaesthesia in a hypopigmented lesion is an Congenital absence of melanocytes General principles of important clue in a clinical diagno- , discoid lupus erythematosus, Acquired destruction of melanocytes management sis of leprosy. Additional investiga- systemic sclerosis (figure 1) Cosmetic camouflage is an import- tions are necessary if the diagnosis ant part of managing hypopig- cannot be confirmed on clinical , phenylketonuria, drugs (eg, Reduced melanin production mented skin lesions. grounds alone. A skin biopsy will skin-whitening creams) It is important to emphasise be useful in some patients. to the patient that, somewhat Tuberous sclerosis Reduced transfer to Idiopathic guttate hypomelanosis counter-intuitively, tanning wors- keratinocytes is often misdiagnosed and treated as ens the cosmetic appearance of pityriasis versicolor. The distinction Post inflammatory hypopigmentation Increased melanin and keratinocyte hypopigmented lesions on fair or may be better elucidated by taking due to psoriasis turnover light skin. It makes the contrast scrapings from the skin lesions in between normal and depigmented question. Scrapings from a lesion of Table 2: Wood’s lamp features in hypopigmentary disorders skin more noticeable. pityriasis versicolor typically have a Furthermore, depigmented skin ‘spaghetti and meatballs’ appearance Hypopigmentary disorder Features under Wood’s lamp has a higher risk for chronic sun under the microscope after dissolv- Pityriasis versicolor Yellow to yellow-green fluorescence damage and skin cancer. This risk ing in 30% potassium hydroxide on of sun damage is heightened in a Vitiligo Bright areas with sharp borders varying in a glass slide. country such as Australia where location and extent As mentioned in Part 1, the use there are long hours of intense of a Wood’s lamp can consider- Tuberous sclerosis Patches; characteristic ash-leaf shape sun. A broad-spectrum sunscreen ably improve the diagnosis of Hypomelanosis of Ito Whorled or streaked patterns. with both UVB and UVA protec- hypopigmentary lesions, especially Naevus anaemicus Lesion becomes inapparent tion helps resist tanning with addi- in patients with lighter skin colour tional protection against chronic (table 2). The features found under Hypochromic naevi Off-white accentuation sun damage.

Vitiligo

VITILIGO is an acquired pig- Table 3: Classification of hypopigmentation/ mentary disorder of the skin and disorders — genetic causes mucous membranes presenting with well-demarcated depig- Extent of disorder Possible causes mented macules of varying sizes Localised Piebaldism and shapes. Depending on the clinical presentation and dis- Ziprkowski–Margolis syndrome tribution, vitiligo can be classi- Hypomelanosis of Ito and mosaicism fied as localised or generalised. Focal dermal hypoplasia Localised disease can be further Naevus depigmentosus classified as focal (one or more Tuberous sclerosis complex macules), segmental (macules in a dermatomal distribution) and Generalised Albinism mucosal (mucous membranes Albinoid disorders (Chédiak–Higashi syndrome, alone). Generalised vitiligo can Griscelli syndrome, Prader–Willi syndrome, be acrofacial (distal fingers and phenylketonuria, homocystinuria) periorificial areas), vulgaris (scattered widely distributed for (tables 3 and 4). For example: be unsatisfactory. Complete patches) or mixed. Universal •  has an ill-defined repigmentation is unlikely in vitiligo refers to extensive and border with slight scaling, usu- most patients and recurrences almost complete depigmentation ally seen on the face in children. are common. Treatment should of the whole body. • Pityriasis versicolor has coalesc- depend on the individual. Patients ing macules with slight scaling. It should be properly counselled Pathogenesis Figure 2: Large anaesthetic hypopigmented macular lesion with raised borders is seen as yellow to yellow-green about the treatment outcome and There are several theories for the due to leprosy. under a Wood’s lamp. side effects. Cosmetic disfigure- pathogenesis of vitiligo. Genetic • Hypopigmented mycosis fun- ment is the main reason for treat- factors may play a role and a posi- anocyte destruction. Vitiligo may vitiligo a mixture of complete and goides has skin atrophy and ill- ment especially in darker skin tive family history is seen in some be associated with other autoim- partial pigmentary loss can be defined lesions. types. Non-treatment is an option patients. There is an absence of mune disorders. seen. There may be associated leu- • Lichen sclerosus et atrophicus in skin type 1 and 2. melanocytes in the lesions, which kotrichia. The lesions may appear has guttate hypopigmentation Topical therapies are suitable is due to the destruction of mel- Diagnosis at sites of trauma from Koebner’s with skin sclerosis. for patients with few lesions. anocytes. Autoimmune mecha- Vitiligo is a clinical diagnosis. phenomenon and this usually indi- • Leprosy has features of anaes- Topical steroid preparations are nisms, cytotoxic mechanisms, Patients may present with progress- cates an active disease. thesia, and has raised borders commonly used as first-line ther- intrinsic defect of melanocytes, ive depigmentation of the skin. The Differentiating vitiligo from (figure 2). apy in localised vitiligo. They oxidant-antioxidant mecha- rate of progression is variable. Usu- other hypopigmented lesions can are moderately successful, but nisms, and neural mechanisms are ally there is complete depigmenta- be difficult sometimes and certain Treatment long-term application can cause thought to contribute to the mel- tion in the lesions but in trichrome specific features should be looked Treatment of vitiligo can often cont’d page 26

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from page 24 Table 4: Classification of hypopigmentation/depigmentation Figure 3: skin atrophy. Topical tacroli- disorders — acquired causes Multiple small mus ointment (0.03% or 0.1%) depigmented Type of Acquired causes is an effective alternative, partic- lesions on the ularly when the disease involves disorder trunk after the head and neck. It can also be Autoimmune Vitiligo, Vogt–Kayonagi syndrome, systemic sclerosis, resolution of the combined with laser and photo- discoid lupus erythematosus inflammatory changes therapy. Vitamin D analogs, cal- Metabolic and Kwashiorkor cipotriol and tacalcitol have been associated nutritional Iron deficiency with pityriasis used as topical therapeutic agents Vitamin B12 deficiency immune-modulating agents for lichenoides Hypopituitarism chronica. the treatment of vitiligo. Hypogonadism Narrow-band UVB photother- Cushing’s apy is commonly used and can be safely used in children and preg- Chemical/drugs Liquid nitrogen, steroid (topical, intralesional, intra-articular) nant or lactating women. Psoralen Bleaching creams photochemotherapy is a good Infections Leprosy Figure 4: A: Test option in patients with widespread Pityriasis versicolor A grafts by mini disease. Psoralens can be given Syphilis punch grafting for localised either topically or orally, followed Post Psoriasis by exposure to artificial UV light stable vitiligo inflammatory Pityriasis alba of the lower lip or natural sunlight. Post-treatment Atopic dermatitis to reintroduce eye protection with UV protective Pityriasis lichenoides chronica (figure 3) colour to a patch sun glasses is necessary. Lesions Melanocytic Halo naevus of vitiligo. B: Test on the face and trunk usually tumours/ Melanoma-associated grafts by mini respond well while lesions on the punch grafting malignancies Mycosis fungoides dorsal surface of the hands show for localised resistance to treatment. Prolonged Other Idiopathic guttate hypomelanosis stable vitiligo treatment over many months is Progressive macular hypomelanosis starting to show required before repigmentation Leucoderma punctata repigmentation appears. Lichen sclerosus et atrophicus on a follow-up visit. Systemic oral steroid (pred- B nisone) is an option in patients unlikely to produce acceptable should be considered in stable with rapidly progressive disease. results. Monobenzyl ether of localised disease and is a good Weekly pulses or lowest effective hydroquinone is used to achieve option in patients with segmen- doses can be given to minimise permanent depigmentation. As tal vitiligo. Even in very stable the side effects. Once the disease the depigmentation is permanent, disease, depigmentation of the is stable it would be desirable to proper counselling is necessary. grafts can occur. Suction epider- change to phototherapy to induce The patient should be started on mal grafting, thin dermoepider- repigmentation. appropriate sun protection meth- mal grafts, noncultured epidermal ods to minimise sun damage of suspensions, cultured Depigmentation therapy totally depigmented skin. suspensions and punch minigraft- Depigmentation therapy will be ing (figure 4) are some methods an option if vitiligo is widespread Surgery that show cosmetically acceptable and repigmentation treatment is Surgical skin-grafting treatments results.

Infective causes

THERE are several infections Figure 5: that may cause hypopigmenta- A A: Pityriasis tion such as pityriasis versicolor versicolor on and leprosy. Other infective causes the left upper include syphilis, other treponema- trunk showing hypopigmented toses and onchocerciasis. macular lesions. B: Pityriasis Pityriasis versicolor versicolor on the Pityriasis versicolor, or tinea ver- thigh showing sicolor, can either be hypopig- hyperpigmented mented or hyperpigmented (figure macular lesions. 5). It is proposed that the hypopig- mentation occurs as a result of the inhibition of tyrosinase by dicar- boxylic acids formed by Malasse- zia furfur. The patients often describe poor tanning of lesions. B Clinical features The pityriasis versicolor lesions are well-demarcated oval to round to the increased risk of liver toxic- macules commonly seen coalesc- ity. Even though it is ing to form irregularly shaped Recurrences can be common rare in Australia, patches. There are fine dust-like even with oral therapy. Hypopig- leprosy should be scales covering the lesions. Wood’s mentation may persist after suc- lamp examination shows yellow- cessful treatment and sometimes suspected in patients ish-white or copper-orange fluo- take months to resolve. who have migrated rescence (table 2). Leprosy from endemic Treatment Even though it is rare in Australia, countries and present Various agents can be used to treat tion on overnight can be helpful in itraconazole are all effective and leprosy should be suspected in pityriasis versicolor. Selenium resistant cases. Topical azole anti- there are different dosing regi- patients who have migrated from with persistent sulfide, sodium sulfacetamide, fungals can be applied every night mens. However, the side effects of endemic countries and present hypopigmented ciclopiroxolamine, azole and for two weeks. Subsequent weekly oral therapy should be discussed with persistent hypopigmented allylamine antifungals have been applications of any of the topical with the patient. Fluconazole lesions. The initial lesion is a lesions. used with success. agents for a few months may help 150-300mg weekly for 2-4 weeks sharply demarcated oval or round There are different topical regi- prevent recurrence. or itraconazole 200 mg daily for hypopigmented macules with dry mens. Selenium sulfide lotion is In patients with widespread seven days are used in extensive scaly centre and erythematous applied daily for two weeks to disease oral antifungal therapy and resistant cases. Ketoconazole borders. Localised anaesthesia and affected areas and washed off after is more convenient and effective. 200mg daily for 10 days is also thickened cutaneous nerves give 10 minutes. Leaving the applica- Ketoconazole, fluconazole and effective but its use is limited due clues to the diagnosis. cont’d page 28

26 | Australian Doctor | 18 April 2014 www.australiandoctor.com.au How To Treat – Disorders of pigmentation— Part 2: Hypopigmentation

Other acquired disorders

Vogt–Koyanagi–Harada Figure 6: Guttate Pityriasis alba usually resolves syndrome hypopigmented spontaneously. Low-potency topi- VOGT–Koyanagi–Harada syn- macules on the cal steroids may help with ery- drome is a rare disease with a pre- shin. thema and pruritus. sumed autoimmune aetiology. It is characterised by chronic, bilat- Post-inflammatory eral granulomatous uveitis with hypopigmentation dermatological, neurological and Post-inflammatory hypopigmen- auditory involvement. The disease tation is more noticeable in dark- has four stages: skinned individuals and can be the • The prodromal stage, where the consequence of both primary cuta- patient has flu-like symptoms neous conditions and secondary to with headache, nausea, menin- therapeutic interventions. These gism, auditory discomfort and may include seborrhoeic derma- tinnitus. titis, pityriasis versicolor, pityria- • Acute uveitic stage. In this stage sis lichenoides, atopic dermatitis, there is onset of blurring of psoriasis, , lichen vision in both eyes and bilateral Figure 7: striatus, cryotherapy, and intral- granulomatous anterior uveitis. Pityriasis alba esional and intra-articular steroid • Convalescent stage, which lesions on the injections (figure 8). The hypopig- occurs several weeks later with face of a child. mentation is attributed to a loss skin changes including vitiligo, of functional melanocytes due to alopecia and poliosis. the inflammation. Repigmenta- • The chronic recurrent stage, tion can take weeks to months. where the patient may subse- The underlying disease should be quently experience repeated treated. Cosmetic camouflage can bouts of uveitis. be maintained until repigmenta- Early diagnosis and steroid tion occurs. therapy help to reduce the com- plications and recurrent attacks. Halo naevus Long-term ophthalmological mon- Halo naevus is also known as itoring is necessary. Skin depig- ‘Sutton naevus’. It is a mole with mentation is treated the same way a white ring, or ‘halo’, around it as vitiligo. (figure 9). They are more common in children and young adults. They Idiopathic guttate hypomelanosis are also seen more commonly in Idiopathic guttate hypomelano- people with multiple melanocytic sis is a benign hypopigmentation naevi. Figure 8: disorder of unknown aetiology. It Depigmentation The halo naevus has a character- is commonly seen in middle-aged on the wrist istic progression. A halo appears women. The lesions are typically following intra- around a pre-existing melano- seen on the anterior lower legs articular steroid cytic naevus and the naevus then initially and gradually spread into injection for disappears gradually. It leaves a the sun-exposed areas (figure 6). de Quervain’s hypopigmented macule that takes The lesions are hypopigmented tenosynovitis. months to repigment. It is consid- or depigmented, discrete, angular ered an autoimmune process. For or circular macules of 1-3 mm in unknown reasons the body reacts diameter. Treatment is mainly against certain moles and make for cosmetic reasons. Topical or them disappear. Usually these intralesional corticosteroids, reti- moles are benign. However, all noids, pimecrolimus have shown halo moles need to be examined variable results. Surgical treat- carefully by a medical practitioner ments with trichloroacetic acid, because malignant melanomas can cryosurgery and dermabrasion have this halo phenomenon. Apart have some success. Fractional car- from the exclusion of a melanoma bon dioxide laser has been a safe and patient reassurance, a halo and effective treatment. mole itself does not require treat- ment. Progressive macular hypomelanosis Hypopigmented mycosis Progressive macular hypomela- Figure 9: Halo fungoides nosis is an uncommon disease in naevi on the Hypopigmented mycosis fungoi- right jaw. Australia but can be commonly des is an atypical, unique vari- seen in patients with skin types ant of mycosis fungoides usually IV-VI. The condition is often observed in dark-skinned individ- misdiagnosed and treated as for uals. It is characterised by gradu- pityriasis versicolor. It is a disease ally progressive hypopigmented of young adults presenting with macules and patches with skin ill-defined asymptomatic hypopig- atrophy. The lesions are com- mented macules on the trunk. monly seen in the trunk. Pruritus The lesions spread slowly and may be a clinical feature. Hypo- coalesce in and around the mid- pigmented mycosis fungoides line. They are more commonly should be included in the differ- seen on the back and can spread ential diagnosis of any persistent to the abdomen. In contrast to hypopigmented macule or patch pityriasis versicolor, progressive that is resistant to treatment. macular hypomelanosis does not Multiple skin biopsies are usu- show scaling. Propionibacterium ally done to obtain a histological acnes causing depigmentation has diagnosis and sometimes repeated been suggested as the causative biopsies after a few months will be factor. needed if the diagnosis remains in Currently 1% clindamycin doubt. Most cases have a benign lotion during the daytime, 5% Pityriasis alba erythema. There can be multiple pigmented mycosis fungoides, course but follow-up of these benzoyl peroxide gel at night-time Pityriasis alba is more commonly lesions on the face (figure 7). The nummular eczema and pityriasis patients will be necessary to detect is commonly used. UVA, UVB seen in children and young adults. upper arms, neck, or shoulders rosea on the face may all mimic recurrences. Hypopigmented or even natural sunlight hastens The disease is characterised by ill- may also be involved. Pruritus pityriasis alba. Atopy and exces- mycosis fungoides responds well repigmentation. Recurrences can defined irregular hypopigmented may be a clinical feature. Pityriasis sive sun exposure can predispose to UVA and UVB, resulting in occur when treatment stops. patches with scaling and mild versicolor, vitiligo, leprosy, hypo- the development of these lesions. long-term remission.

28 | Australian Doctor | 18 April 2014 www.australiandoctor.com.au Lichen sclerosus Asymptomatic Figure 10: surface of the plaque there are Lichen sclerosus, or lichen scle- Extragenital comedo-like plugs and telangiec- rosus et atrophicus, is a chronic extragenital lichen lichen tasia that may be easily identified inflammatory dermatosis of the sclerosus usually sclerosus with dermoscopy and is a useful skin presenting as white plaques showing clue to differentiate it from other with epidermal atrophy, scarring does not require any guttate hypopigmented lesions. With time, and skin sclerosis. Lichen sclerosus treatment. hypopigmented the plugs will disappear and leave has both genital and extragenital atrophic a smooth, porcelain-white plaque. plaques in the presentations. Extragenital lichen The size of the lesions can range trunk. sclerosus is usually asymptomatic from a few millimetres to very (figure 10). Vulvar lichen sclero- large areas. A skin biopsy can con- sus usually presents with atrophic firm the clinical diagnosis. hypopigmented lesion, pruritus, Asymptomatic extragenital dyspareunia, dysuria or genital lichen sclerosus usually does not bleeding. Penile lichen sclerosus is require any treatment. Super- usually pruritic and the skin scle- potent topical steroids, topical rosis later results in phimosis. testosterone, topical retinoids, Lichen sclerosus in the skin usu- tacrolimus and pimecrolimus have ally starts as white papules that proven useful in treating female coalesce into plaques. On the genital lichen sclerosus.

Genetic and congenital disorders

Albinism Figure 11: tion. Treatment is not required for ALBINISM is a group of inherited A baby with naevus anaemicus. Camouflage disorders of melanin synthesis and hypomelanosis makeup may help cover the lesion. is characterised by a congenital of Ito on the reduction or absence of melanin trunk. Achromic naevus (naevus pigment in the skin, hair and eyes. depigmentosus) There are two types of albinism: Achromic naevus is usually a solitary ocular cutaneous albinism and hypopigmented macule seen from . Ocular albinism birth or early childhood. The lesions only affects the optic system and are well defined with irregular bor- does not affect the skin and hair ders resembling a splash of paint. colour. Achromic naevus appears off- In ocular cutaneous albinism, white on Wood’s lamp examina- there is a reduction or absence of tion. Excimer laser, phototherapy melanin in the skin, hair and eyes. and skin grafting have been tried The lack of skin pigment results for the treatment but reassurance in a pale skin appearance and an is generally adequate. increased risk of skin cancer. Ocu- lar cutaneous albinism is divided Tuberous sclerosis further into several subtypes based Tuberous sclerosis or tuberous on the genetic mutation. Chédiak– sclerosis complex is a neurocuta- Higashi syndrome is a rare autoso- neous disorder that causes hamar- mal recessive disorder that has an Patients with ocular multiple symmetrical hypopig- as a hypopigmented macule or tomas in various organs including associated with mented or depigmented macules. patch since birth that grows with the skin. Ash-leaf hypopigmented ocular cutaneous albinism. cutaneous albinism The lesions are commonly seen on the child. It is a pale macule with macules are usually the only lesion Patients with ocular cutane- should be referred to the face; the trunk and extremi- irregular margins and persists seen at birth. Ash-leaf macules can ous albinism should be advised ties are also involved. The skin throughout life. Diascopy helps be multiple and become prominent to apply broad-spectrum sun- an ophthalmologist lesions can mimic vitiligo. Piebald- to differentiate naevus anaemicus when examined under Wood’s screens with an SPF of at least 30, and regularly ism is a benign disorder. However, from vitiligo and hypochromic lamp. together with other methods that patients are at risk for actinic dam- naevi. This test involves apply- prevent sun exposure. Eyes should screened for skin age. Cosmetic camouflage and sun ing pressure on a skin lesion with Hypomelanosis of Ito be protected by wearing dark, UV- cancers. protection are important aspects a glass slide and observing for Hypomelanosis of Ito presents as blocking sunglasses. They should in the management. Skin grafts a colour change. When applied hypopigmented whorls of skin be referred to an ophthalmologist are effective and stable. Piebald- to naevus anaemicus it becomes along the Blaschko lines (figure 11) and regularly screened for skin ism is one of the cutaneous signs indistinguishable from the sur- and can be associated with neuro- cancers. of Waardenburg syndrome, along rounding skin as the surrounding logical, skeletal, hair and dental with heterochromia of the irides, skin is blanched with pressure. defects. The skin lesions present Piebaldism lateral displacement of inner can- Wood’s lamp examination does from birth and are asymptomatic. Piebaldism is a rare autosomal thi, and deafness. not accentuate naevus anaemicus Hypopigmented macules along the dominant disorder caused by the and may make the lesion inappar- lines of Blaschko are seen some- congenital absence of melano- Naevus anaemicus ent, whereas in vitiligo the lesions times involving more than one cytes. The patient typically pre- Naevus anaemicus is a congeni- become prominent and hypochro- dermatome. Wood’s lamp exam- sents with white forelock and tal vascular anomaly presenting mic nevi show off-white accentua- ination enhances the pattern.

Case study

DILAN, a 21-year-old medical Figure 12: lesions spread despite the treat- student, was referred by his GP to Progressive ment and he had not applied any the dermatology clinic with hypo- macular further treatment over the past pigmented lesions on the trunk for hypomelanosis two months. over six months. His mother had on the back with Dilan was worried because the hypopigmented noted the lesions first when they lesions were spreading, and he macular lesions were on his back. These were then coalescing in was ashamed to take his shirt off observed to spread towards the and around the to swim. shoulders and the lateral abdo- midline. On examination, there were men. There is no itching or any hypopigmented macules on other symptoms associated with the back, shoulders and lateral the lesions. He had had the lesions abdominal wall. The lesions coa- for over two months before he pre- lesced at the midline, forming large sented to the GP. macules. There was no visible scal- The GP gave him topical 2% ing (figure 12). The lesions were ketoconazole cream to be applied not anaesthetic. Scrapings from twice a day for four weeks. The cont’d next page

www.australiandoctor.com.au 18 April 2014 | Australian Doctor | 29 How To Treat – Disorders of pigmentation— Part 2: Hypopigmentation

from previous page Dilan was advised to expose the appearance and progressive nature Online resources the lesions for pityriasis versicolor lesions to natural sunlight around cause distress in affected patients. Conclusion were negative. 10-11am for 10-15 minutes so that Careful examination of its distribu- eMedicine A diagnosis of progressive macu- he could hasten repigmentation of tion on the back — with the lesions HYPOPIGMENTATION dis- www.emedicine.com/derm/ lar hypomelanosis was made. The the lesions. He had a good response coalescing in the midline, an absence orders, while often not as cos- benign nature of the condition was after four weeks but he was asked to of any scaling, and a slowly progres- metically common in Australia as DermNet NZ explained to Dilan. He was started continue the treatments for another sive nature towards the anterior hyperpigmentary disorder, may dermnetnz.org on 1% clindamycin gel in the morn- four. abdominal wall — helps to differen- cause as much psychological dis- ing and 5% benzoyl peroxide gel at Progressive macular hypomela- tiate it from many similar hypopig- tress to the patient as hyperpig- night to be continued for 4-8 weeks. nosis is a benign condition but its mented lesions. mentary disorders. Some of the Further reading hypopigmentary disorders will 1. Wolff K, et al. Fitzpatrick’s Dilan was advised also be associated with an underly- Dermatology in General Medicine. ing systemic disease and a reason- 7th edn. McGraw-Hill Inc, New to expose the lesions able level of suspicion is required York, 2007. to natural sunlight to pick up acquired causes of 2. James WD, et al. Andrews’ hypopigmentation such as hor- Diseases of The Skin: Clinical around 10-11am for monal disorders and vitamin defi- Dermatology. 11th edn. Elsevier 10-15 minutes so ciencies. A thorough history and Inc., Edinburgh, 2011. clinical examination will guide 3. Burns T, et al. Rook’s Textbook that he could hasten appropriate investigations and of Dermatology. 8th edn. Wiley- repigmentation of the prompt referral to the specialist if Blackwell, Hoboken NJ, 2010. it is required. It should be remem- lesions. bered that regardless of whether the underlying cause is able to be References cured, cosmetic camouflage, sun Available on request from protection and psychosocial supp- [email protected] ort are important principles in the management of these conditions.

Instructions Complete this quiz online and fill in the GP evaluation form to earn 2 CPD or PDP points. How to Treat Quiz We no longer accept quizzes by post or fax. Disorders of pigmentation— Part 2: The mark required to obtain points is 80%. Please note that some questions have more than one correct answer. GO ONLINE TO COMPLETE THE QUIZ Hypopigmentation — 18 April 2014 www.australiandoctor.com.au/education/how-to-treat

1. Which TWO statements are correct c) Vitiligo is indistinguishable from lichen regarding the clinical features of acquired c) Achromic naevus lesions resemble a splash regarding the general approach to and sclerosus hypopigmentary disorders? of paint management of skin hypopigmentation? d) Vitiligo patches that appear at sites of trauma a) Vogt-Koyanagi–Harada syndrome presents d) Hypopigmented lesions in tuberous sclerosis a) History of a preceding rash or anaesthesia indicates an active disease initially like a flu with uveitis usually present as large papulotubercles over a hypopigmented lesion can both point b) Idiopathic guttate hypomelanosis is to a diagnosis 4. Which TWO statements are correct commonly seen on the anterior lower legs of 9. Joshua is a 56-year-old man who returned b) Skin scrapings for mycology are not useful in regarding the treatment of vitiligo? middle-aged women recently from India after a six-month the diagnosis of skin hypopigmentation a) Vitiligo should be treated with weekly high- c) Genital lichen sclerosus usually presents medical mission. He had developed several c) Sunscreens should not be applied dose prednisone orally until repigmentation with asymptomatic atrophic hypopigmented pruritic hypopigmented lesions on his to depigmented skin lesions to avoid occurs lesions trunk. Which TWO statements are correct exacerbating the problem b) Surgery with skin grafts may be a good option d) Hypopigmented mycosis fungoides is usually regarding his assessment and diagnosis? d) Cosmetic camouflage can aid management of for stable segmental vitiligo a clinical diagnosis based on asymptomatic a) Skin atrophy and ill-defined lesions may point hypopigmented skin lesions c) Depigmentation therapy is used for small persistent hypopigmentation on the digital to hypopigmented mycosis fungoides areas of localised vitiligo webs b) Leprosy may be diagnosed clinically based on 2. Which THREE statements are correct d) Phototherapy for repigmentation of vitiligo the history of a prolonged stay in an endemic regarding the Wood’s lamp features of requires treatment over many months 7. Which TWO statements are correct area hypopigmentary disorders? regarding the management of acquired c) Dermoscopic findings of comedo-like plugs a) Wood’s lamp examination of pityriasis 5. Which TWO statements are correct hypopigmentary disorders? and telangiectasia may suggest the diagnosis versicolor shows dark areas with silver regarding the diagnosis and management a) Apart from reassurance a halo naevus does of psoriasis borders of pityriasis versicolor and other infective not require further management d) Differential diagnoses include syphilis and b) Wood’s lamp examination of vitiligo shows causes of hypopigmentation? b) Pityriasis alba is self-limiting and usually nutritional deficiency bright areas with sharp borders a) Lesions of pityriasis versicolor are usually resolves spontaneously c) Wood’s lamp examination of hypochromic covered by fine dust-like scales c) Asymptomatic extragenital lichen sclerosus 10. Skin biopsies confirmed a diagnosis of naevi shows off-white accentuation b) Hypopigmentation generally clears usually does not require any treatment hypopigmented mycosis fungoides. Which d) Naevus anaemicus under the Wood’s lamp immediately after successful treatment of the d) Cosmetics should not be applied to post- TWO statements are correct regarding becomes inapparent underlying infective cause inflammatory hypopigmentation Joshua’s ongoing management? c) Other infections that may causes skin a) Topical antifungal treatment is effective in 3. Which TWO statements are correct hypopigmentation include syphilis and 8. Which TWO statements are correct 30% of cases regarding the clinical features and onchocerciasis regarding genetic or congenital causes of b) Ultraviolet therapy is effective in achieving diagnosis of vitiligo? d) Oral ketoconazole is safe and may be given hypopigmentation? long-term remission a) A skin biopsy is necessary to confidently for a few months to prevent recurrence of a) Skin lesions in hypomelanosis of Ito develop c) Follow-up is not necessary after resolution of diagnose vitiligo pityriasis versicolor along the lines of Blaschko the hypopigmentation b) Vitiligo lesions may not be completely b) Naevus anaemicus becomes erythematous d) Joshua may be reassured that his condition depigmented 6. Which TWO statements are correct on diascopy will most likely be benign

CPD QUIZ UPDATE The RACGP requires that a brief GP evaluation form be completed with every quiz to obtain category 2 CPD or PDP points for the 2014-16 triennium. You can complete this online along with the quiz at www.australiandoctor.com.au. Because this is a requirement, we are no longer able to accept how to treat Editor: Dr Steve Liang the quiz by post or fax. However, we have included the quiz questions here for those who like to prepare the answers before completing the quiz online. Email: [email protected]

Next week Zoonoses are infections or infectious agents transmitted from vertebrate animals to humans. The next How to Treat discusses the common zoonoses — Q fever, leptospirosis and brucellosis – and several more uncommon conditions that should be considered in patients who present with unusual symptoms after having been in rural Australia and/or having had close contact with farm animals. The author is Associate Professor Neil Parker, adjunct associate professor, school of public health, tropical medicine and rehabilitation sciences, James Cook University, Townsville, Queensland.

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