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Vitiliginous Lesions Induced by Amyl Nitrite Exposure

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Vitiliginous Lesions Induced by Amyl Nitrite Exposure Vitiliginous Lesions Induced by Amyl Nitrite Exposure Kathleen Vine, MD; Marc Meulener, MD, PhD; Sherry Shieh, MD; Nanette B. Silverberg, MD Chemical (or contact) leukoderma is a condi- chemical exposure rather than spreading beyond the tion induced by local cutaneous exposure to directly exposed skin.1 chemicals or medicaments that are toxic to mela- Many exogenous agents are used to lighten the nocytes and/or koebnerize preexisting vitiligo skin and hair. The most commonly prescribed medi- vulgaris. Chemicals known to induce leukoderma cations used to lighten or bleach the skin are hydro- include phenol/catechol derivatives (eg, hydro- quinone and its derivatives (ie, monobenzyl ether, quinone), sulfhydryls, contact sensitizing agents monomethyl ether, monoethyl ether).2,3 Chemical (eg, squaric acid dibutylester), and more recently leukoderma primarily has been described in vitiligo imiquimod, among others. We report the case of patients who use ammonia-based hair dyes, which a 37-year-old black man with human immunodefi- have been found to be toxic to melanocytes, result- ciency virus who developed chemical leukoderma ing in decreased or absent cutaneous pigmentation.4 in the nasal and perioral areas within 4 weeks Other agents have been shown to induce leukoderma of spilling liquid amyl nitrite, which he had been or vitiligo in patients following topical application, inhaling as a recreational drug,CUTIS on his lower face. intralesional injection, or oral ingestion (Table).59 The depigmented regions were treated with a Treatment of chemical leukoderma involves discon- biweekly regimen of 308-nm excimer laser treat- tinued application of the offending agent(s) and use ment for a total of 78 sessions. More than 90% of topical vitiligo therapies. We report a case of facial cutaneous repigmentation was achieved. Amyl chemical leukoderma following exposure to liquid nitrite–induced vitiliginous lesions are rare. We amyl nitrite. The patient was successfully treated also discuss potential mechanisms of hypopig- with an excimer laser. mentationDo from chemical agentsNot and therapeutic Copy options for chemical leukoderma. Case Report Cutis. 2013;91:129-136. A 37-year-old black man with human immunodefi- ciency virus (CD4 lymphocyte count, 924 cells/mm3; undetectable viral load) and seasonal allergies pre- hemical (or contact) leukoderma is the physi- sented with acute-onset facial depigmentation of cal lightening or depigmentation of skin 3 months’ duration. The patient did not have a his- Cor hair following exposure to an exogenous tory of vitiligo or other pigmentation disorders; he chemical. The clinical appearance of chemical leu- had no family history of vitiligo. He reported twice koderma may resemble a localized area of vitiligo but weekly recreational inhalation of amyl nitrite fumes differs from contact/occupational vitiligo in that the for the last 3 to 4 years. Two months prior to pre- depigmentation is confined to the area(s) of initial sentation, the patient had accidentally spilled liquid amyl nitrite on the skin of the nasal and maxillary regions as well as the right nasolabial fold. Over 4 weeks the affected area began to peel, exposing “red, cracking skin” that was “sore, painful, itchy, and dry,” From the Department of Dermatology, St. Luke’s-Roosevelt according to the patient. Following localized facial Hospital Center, New York, New York, and Beth Israel Medical skin peeling, the affected areas healed with depig- Center, New York. mentation. The patient presented to the dermatology The authors report no conflict of interest. Correspondence: Nanette B. Silverberg, MD, Department of department seeking therapies for repigmentation. Dermatology, St. Luke’s-Roosevelt Hospital Center, 1090 Amsterdam Physical examination revealed well-demarcated Ave, Ste 11D, New York, NY 10025 ([email protected]). depigmented patches along the distal nasal tip, nasal WWW.CUTIS.COM VOLUME 91, MARCH 2013 129 Copyright Cutis 2013. No part of this publication may be reproduced, stored, or transmitted without the prior written permission of the Publisher. Amyl Nitrite–Induced Vitiliginous Lesions Mechanisms of Depigmentation for Known Select Compounds Specific Mechanism Category of Action Topical Compound/Trauma Other Pertinent Effects Pre–melanin Decreased tyrosinase Tretinoin5 Unknown synthesis transcription pathway MITF downregulation Lysophosphatidic acid6; C2 Unknown ceramides7; vitamin E8 9 10 Increased destruction Phospholipase D2 ; fatty acids Unknown of tyrosinase Inhibition of tyrosinase Glycosphingolipids11 Unknown maturation Inhibition Inhibition of tyrosinase via Phenol/catechol derivatives Oxidative stress–mediated of melanin alternative substrate (hydroquinone,12 melanocytotoxic effect synthesis 4-hydroxyanisole,13 monobenzone14) 4-S-cysteaminylphenol and Melanocytotoxicity via CUTIS4-S-cysteinylphenol15 alkylation of cell proteins Resveratrol16 ROS scavenger; COX-2 inhibitor; anticancer activity Aloesin17 Noncompetitive inhibition of tyrosine hydroxylase Do NotAzelaic acid18 CopyUnknown Copper chelation (required Kojic acid19; methyl gentisate20 Antioxidant activity; iron for tyrosinase activity) chelator; NF-kB inhibition Peroxidase inhibition Ellagic acid21; ascorbic acid Scavenger activity (vitamin C)22 Glucocorticoids22 Unknown Inhibition of Koebnerization of vitiligo Serine protease inhibitors23,24; Unknown 25 26 melanosome due to irritant reaction or niacinamide (vitamin B3) ; lectins ; transfer trauma neoglycoproteins26 Melanocyte Irritation/traumatic Tazarotene27; eyebrow plucking28; Unknown loss (vitiligo (koebnerization) striae29-31; radiotherapy32; laser or complete resurfacing33; scratching34 chemical leukoderma) 130 CUTIS® WWW.CUTIS.COM Copyright Cutis 2013. No part of this publication may be reproduced, stored, or transmitted without the prior written permission of the Publisher. Amyl Nitrite–Induced Vitiliginous Lesions Specific Mechanism Category of Action Topical Compound/Trauma Other Pertinent Effects Melanocyte Autoimmune activation of Imiquimod35,36 Unknown loss (vitiligo TLR-7/TLR-8 pathway or complete chemical Allergic contact dermatitis Phenols/catechols1,37 (paratertiary- Unknown leukoderma) amyl-phenol,38 p-tert-butylphenol,39 (continued) monomethyl/monobenzyl ether40); sulfhydryls1; cinnamic aldehyde41; alstroemeria42; squaric acid dibutylester43; carbyne44; cerium oxide45; diphencyprone46; nickel47; paraphenylenediamine48; primula49; arsenic50; chloroquine51; thiotepa52; physostigmine53; prolixin54 Unknown Imatinib55-58 Unknown Abbreviations: MITF, microphthalmia-associated transcription factor; ROS, reactive oxygen species; COX-2, cyclooxygenase 2; NF-kB, nuclear factor kB; TLR, toll-like receptor.CUTIS alae, philtrum, and right nasolabial fold and maxilla therapy for a total of 78 sessions and achieved com- following a splash pattern of amyl nitrite exposure plete facial repigmentation. (Figure, A and B). No nasopharyngeal mucosal lesionsDo or ulcerations were Notpresent. No cervical Comment Copy lymphadenopathy was palpated. The patient was Vitiligo is the loss of cutaneous pigment caused by unwilling to undergo amyl nitrite patch testing or reduced melanin production, inactivity of pigment laboratory screening for glucose-6-phosphate dehy- cells, and/or melanocyte destruction. Pigmentary dis- drogenase (G6PD) deficiency. orders can cause substantial psychological impairment After topical treatments with tacrolimus oint- in patients.60 ment 0.1% and moisturizers were unsuccessful, a Unlike vitiligo, chemical leukoderma is an biweekly regimen of 308-nm excimer laser (XTRAC, acquired hypomelanosis caused by chemical expo- PhotoMedex) treatments was started. The initial sure, especially to phenol derivatives and sulfhydryls, laser setting was 100 mJ/cm2 with a treatment area of which inhibit or interfere with melanin biosynthe- 100 cm2; dose strength was increased by 10% to 15% sis and dispersal.2 Several potential mechanisms of per session until session 20, at which point a fixed hypopigmentation for a number of chemical agents dose of 320 mJ/cm2 was administered at each subse- have been proposed (Table); based on our case, we add quent session. The treatments were well tolerated by chemical destruction of melanocytes and koebneriza- the patient. Evidence of perifollicular repigmentation tion of vitiligo within areas of chemically damaged was observed following the third treatment; with skin. The latter mechanism is the primary cause of each successive treatment, repigmentation increased complete leukoderma, as opposed to the partial leu- and the remaining areas of facial depigmentation koderma induced by topical hydroquinones in the decreased (Figure, C–F). Following roughly 42 treat- absence of vitiligo. ment sessions, the depigmentation was almost com- Alkyl nitrites such as amyl nitrite pletely resolved and the patient was satisfied with (CH3[CH2]4ONO2), butyl nitrite, and isopropyl nitrite the cosmetic results. He continued the excimer laser are illegal recreational drugs (referred to as “poppers” or WWW.CUTIS.COM VOLUME 91, MARCH 2013 131 Copyright Cutis 2013. No part of this publication may be reproduced, stored, or transmitted without the prior written permission of the Publisher. Amyl Nitrite–Induced Vitiliginous Lesions A B CUTIS Do NotC Copy D E F Depigmented patches involving the nasolabial folds, philtrum, columella, and nasal alae after exposure to liquid amyl nitrite (A and B). After 12 treatments with an excimer laser, follicular repigmentation was observed (C and D);
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