Contact depigmentation following irritant contact ...

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aggravated myopia is unknown at present, but corneal steepening has been reported after relatively shortterm isotretinoin use[6] and may cause this error of refraction. Although keratometry or corneal topography was not done in this patient, we can only presume that the two-month delay in consulting an ophthalmologist probably caused permanent steepening of the cornea. In previous reports, myopia resolved when the drug was stopped early, but not if there was a delay, which points towards a potentially reversible change in the refractive apparatus of the eye. With this report, we wish to sensitize the dermatologist community to this uncommon visual side effect of isotretinoin. A comprehensive history of previous eye complaints should always be taken before starting this drug so that any deterioration in visual acuity of patients using it can be picked up early and the drug stopped to avoid a permanent refractive error.

Abir Saraswat Indushree Skin Clinic, Lucknow, India Address for correspondence: Dr. Abir Saraswat, Indushree Skin Clinic, B 7, Indira Nagar, Lucknow 226 016, India. E-mail: [email protected] Access this article online Quick Response Code:

Website: www.ijdvl.com DOI: 10.4103/0378-6323.84083 PMID: *****

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Fraunfelder FW. Ocular side effects associated with isotretinoin. Drugs Today (Barc) 2004;40:23-7. Fraunfelder FT, Fraunfelder FW, Edwards R. Ocular side effects possibly associated with isotretinoin usage. Am J Ophthalmol 2001;132:299-305. Heuberger A, Buchi ER. Irreversible cataract as a possible side effect of isotretinoin. Klin Monatsbl Augenheilkd 1994;204:465-7. Palestine AG. Transient acute myopia resulting from isotretinoin (accutane) therapy. Ann Ophthalmol 1984;16:660,662. Martínez-González MC, García-Silva J, Sánchez MA, Castiñeiras I, del Pozo J, Capdevila EF. Acute myopia while on isotretinoin treatment. J Eur Acad Dermatol Venereol 2007;21:977-8. Santodomingo-Rubido J, Barrado-Navascués E, RubidoCrespo MJ. Drug-induced ocular side-effects with isotretinoin. Ophthalmic Physiol Opt 2008;28:497-501.

Contact depigmentation following irritant contact dermatitis to chloroxylenol (dettol) Sir, Contact de-pigmentation or chemical leukoderma can occur as sequelae of either irritant or allergic contact dermatitis (ACD) that may or may not be of occupational origin. The chemicals implicated invariably are monobenzyl ether of hydroquinone, hydroquinone, tertiary butyl catechol, p-tertiary butyl phenol (PTBP), p-cresol, phenol derivatives, mercaptoamines, physostigmine, and topical minoxidil.[1,2] The described case of contact depigmentation following irritant contact dermatitis (ICD) from chloroxylenol (dettol), a common household disinfectant, is first of its kind to the best of our knowledge. A 65-year-old male presented with mild erythema and scaling, hyperpigmented, and depigmented patches of variable size and shape over face, ears, “V” area of neck and dorsal of hands and feet [Figure 1]. He had applied undiluted chloroxylenol (dettol) over face, hands, and feet for itchy skin (photopruritus) and developed erythema, edema, oozing, crusting, and stinging and burning sensation that subsided over next 2 weeks with blotchy hyperpigmentation and depigmentation. He did not have history of prior topical/systemic medications or, personal or family history of vitiligo. Systemic examination and laboratory investigations were normal. A skin biopsy performed with the provisional diagnoses of contact depigmentation and disseminated discoid lupus erythematosus showed focal hyperkeratosis, epidermal atrophy, flattened reteridges, perivascular lymphocytic infiltrate in the upper dermis and lack of melanocytes in the basal layer. Patch testing showed no positive reaction with Indian Standard Series[3] or chloroxylenol (1% pet), but an irritant reaction to undiluted chloroxylenol occurred [Figure 2] and the test site developed depigmentation later. Topical mometasone furate 0.1% ointment was prescribed for twice daily application. Chemical leukoderma from occupational exposure to compounds containing PTBP, amylphenol, O-syl, vesprene in insecticides, paints, rubber, lubricating and motor oils, photographic chemicals, antimicrobials,

Indian Journal of Dermatology, Venereology, and Leprology | September-October 2011 | Vol 77 | Issue 5



a

b

Figure 1: (a and b) Widespread depigmentation of “V” area of neck and acro-facial skin 2 weeks after acute irritant contact dermatitis to chloroxylenol

especially in perineal area, or for any other dermatoses such as urticaria, generalized pruritus, xerosis, or inflammatory conditions without medical advice. It is a potential contact sensitizer and can cause localized ICD, ACD or exacerbation of pre-existing dermatitis.[8] Generalized body involvement may occur from its use in bathing water or for washing particularly when used undiluted. However, chemical leukoderma due to chloroxylenol (dettol) is rare. Malakar and Panda[9] reported widespread hypopigmentation in a car mechanic who took dettol bath on two consecutive days to treat a pustular dermatosis and developed generalized depigmentation a week later. A positive patch test to chloroxylenol (1%) and depigmentation at the patch test site in their patient suggested contact allergic dermatitis to chloroxylenol as the underlying mechanism. Negative reaction with chloroxylenol (1% in petrolatum), irritant contact reaction to undiluted chloroxylenol (as used by the patient) on patch testing and subsequent depigmentation of test site, and histologic features were suggestive of chemical leukoderma as a result of ICD in our patient. As he did not follow-up further, his primary dermatosis (cause of photopruritus?) remained unidentified.

Ghanshyam K. Verma, Vikram K. Mahajan1, Vinay Shanker, Geeta Ram Tegta, Nidhi Jindal, Samridhi Minhas Figure 2: Patch-testing shows an irritant reaction to undiluted chloroxylenol

disinfectants, soaps, detergents, deodorants, and inks has been reported often.[1] Nonoccupational chemical leukoderma reportedly occurs secondary to allergic contact dermatitis with para phenylene diamine (PPD) in hair colorants or temporary tattoos,[4,5] methacrylates,[6] perfumes, and alstroemeria[7] or following contact with common household products such as rubber or nylon articles, spectacles, plastic watch strap, adhesives, condoms, foot wears, etc.[1] Chloroxylenol (dettol) or p-chloro-m-xylenol (PCMX), a water and oil soluble halogenated aromatic compound, is used commonly as preservative and household disinfectant or as an active agent in antimicrobial soaps. It is also used in many over-the-counter products for cuts, wounds and infections, powders, cleansers, work creams, coolant oils, electrocardiogarphic pastes and cosmetics. People often use it diluted/undiluted to decontaminate themselves or their environment hoping to eradicate a genuine or imagined infection, add in bathing water, apply it in inflammatory conditions

Department of Dermatology, Venereology and Leprosy, Indira Gandhi Medical College, Shimla 171 001, Himachal Pradesh, 1Department of Dermatology, Venereology and Leprosy, Dr. R.P. Govt. Medical College, Kangra (Tanda) 176 001, Himachal Pradesh, India Address for Correspondence: Dr. Vikram K. Mahajan, Department of Dermatology, Venereology and Leprosy, Dr. R.P. Govt. Medical College, Kangra (Tanda) 176 001, Himachal Pradesh, India. E-mail: [email protected] Access this article online Quick Response Code:

Website: www.ijdvl.com DOI: 10.4103/0378-6323.84086 PMID: *****

REFERENCES 1.

2. 3.

Dutta AK, Dutta PK, Dhar S. Pigmentary disorders: chemical induced disorders. In: Valia RG, Valia AR, editors. IADVL Textbook and Atlas of Dermatology, 2nd ed. Mumbai (India): Bhalani Publishing House; 2001. p. 604-5. Malakar S, Dhar S. Leukoderma associated with topical minoxidil: A report of two cases. Dermatology 2000;201:183-4. Sharma VK, Sethuraman G, Garg T, Verma KK, Ramam M.

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4. 5. 6. 7. 8. 9.

Patch testing with the Indian standard series in New Delhi. Contact Dermatitis 2004;51:319-21. Bajaj AK, Gupta SC, Chatterjee AK, Singh KG, Basu S, Kant A. Hair dye depigmentation. Contact Dermatitis 1996;35:56-7. Nikkels AF, Henry F, Piérard GE. Allergic reactions to decorative skin paintings. J Eur Acad Dermatol Venereol 2000;15:140-2. Casse V, Salmon-Ehr V, Mohn C, Kalis B. Chronic depigmentation due to positive patch tests for methacrylate derivatives. Ann Dermatol Venereol 1998;125:56-7. Björkner BE. Contact allergy and depigmentation from alstroemeria. Contact Dermatitis 1982;8:178-84. Berthelot C, Zirwas MJ. Allergic contact dermatitis to chloroxylenol. Dermatitis 2006;17:156-9. Malakar S, Panda S. Post inflammatory depigmentation following allergic contact dermatitis to chloroxylenol. Br J Dermatol 2001;144:1275-6.

Psoriasiform skin eruption associated with sorafenib therapy Sir, Sorafenib is an oral multi-targeted kinase inhibitor with anti-angiogenic and anti-proliferative activity.[1] It is approved for treatment of unresectable hepatocellular carcinoma and advanced renal carcinoma. Sorafenib acts by inhibition of several receptor tyrosine kinases, such as vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR), c-kit and the intracellular Raf kinase (Raf-1).[1] Cutaneous toxicity is relatively common in patients receiving sorafenib. The most frequent cutaneous side effect is the hand-foot syndrome; other described adverse skin reactions include facial erythema, acral erythema, erythema multiforme, subungual splinter hemorrhage, stomatitis, and alopecia.[1] Recently, two cases of sorafenib-associated psoriasiform eruption have been reported.[1,2] Furthermore, exacerbation of psoriasis was also described after treatment with the EGFR tyrosine kinase inhibitor gefitinib.[3] Moreover, a case of psoriasiform plaques histopathologically suggestive of acute generalized exantematous pustulosis have also been reported with lapatinib, another multikinase inhibitor.[4] We present herein an additional case of a patient who developed cutaneous psoriatic lesions following sorafenib therapy. A 59-year-old man was diagnosed of nodular hepatocellular carcinoma secondary to alcoholic liver cirrhosis in July 2009. The tumor was surgically excised. In November 2009, multiple lung metastases were detected bilaterally on chest CT scan. Sorafenib 400 mg orally twice daily was then initiated with a good clinical response. In March 2010, 4 months later, he 614

developed an extensive cutaneous eruption involving the trunk and limbs. The patient had no personal or family history of psoriasis, and he was not receiving simultaneously any other medication. Dermatological examination revealed multiple erythematous, scaly, papules and plaques on the thorax, abdomen, back, and proximal areas of the limbs. The psoriasiform lesions were mainly of guttate type and showed Koebner´s phenomenon [Figure 1]. A skin biopsy specimen disclosed psoriasiform hyperplasia of the epidermis with confluent parakeratosis and dilated vessels in the papillary dermis, consistent with psoriasiform eruption [Figure 2]. Despite this side effect, sorafenib therapy was continued because the drug was effective in the control of the metastatic progression. The cutaneous lesions improved significantly after treatment with topical steroids and narrow-band UVB phototherapy. The development of psoriasiform eruptions in patients treated with sorafenib seems paradoxical, since this

Figure 1: Multiple psoriasiform lesions mainly of the guttate type on the trunk that show Koebner´s phenomenon

Figure 2: The epidermis showed a psoriasiform hyperplasia with confluent parakeratosis. (H and E, ×100)

Indian Journal of Dermatology, Venereology, and Leprology | September-October 2011 | Vol 77 | Issue 5

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