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Vitiligo is an autoimmune disease characterized by depigmentation of the skin due to destruction of melanocytes. Interferons have been used for the treatment of chronic hepatitis C and some malignancies. We report interferon alpha-2a-induced vitiligo in a male patient with chronic active hepatitis C. All skin lesions disappeared completely without requiring therapy after discontinuation of interferon. This case suggests that vitiligo may be developed during interferon therapy as a side effect. Halis Simsek, MD, Hacettepe University Medical School, Section of Gastroenterology, Ankara (Turkey) Introduction Vitiligo is an acquired dermatologic disorder characterized by local, dispersed or diffuse depigmented patches on the skin caused by disappearance of functional melanocytes [1]. The interferons (IFNs) are natural proteins with antiviral, antitumoral and immu-nomodulating functions. They have been successfully used for the treatment of chronic hepatitis C [2]. Several autoimmune side effects of IFN treatment including thyroid dysfunction and psoriasis are reported [3,4]. Interferon-induced vitiligo was previously .reported in IFN-containing combination chemotherapy regimes for melanoma [5]. Recently, a case of alopecia followed by development of canities and vitiligo has been reported 3 months after discontinuing alpha-INF therapy [6]. We report a case of IFN induced vitiligo during therapy of chronic hepatitis C. Case Report A 39-year-old asymptomatic male with a previous history of blood transfusions was referred to our hospital because of elevated serum transaminases levels. He did not have any personal or family history of autoimmune diseases. Physical examination was unremarkable except for a hepatomegaly of 2 cm. Laboratory analysis of blood showed a serum alanine aminotransferase level of 219 IU/ml, aspartate aminotransferase of 64 IU/ ml. Hepatic markers were negative with the exception of antihepatitis C virus antibody positivity. A high level of liver enzymes continued for a 6-month follow-up and a percutaneous liver biopsy confirmed the diagnosis of chronic hepatitis C infection. Recombinant IFN alpha-2a (Roferon, Roche) treatment was started at a D ow nl oa de d by : 54 .7 0. 40 .1 1 11 /2 0/ 20 17 9 :0 6: 03 P M dose of 3 MIU, s.c. 3 times a week. One month later, hypoand depigmented macules developedin the anterior area of the patient’s neck. A diagnosis of vitiligo was made and localcorticosteroid ointment was applied. Partial improvement was observed on the skin lesions withthis local treatment during IFN therapy. But all skin lesions healed completely without requiringany corticosteroid therapy after discontinuation of IFN and the patient was followed up foranother 10 months free of vitiligo.DiscussionVitiligo is an acquired, idiopathic hypo-melanotic disease characterized by circumscribeddepigmented macules. Despite several investigations the cause of vitiligo still remains unknown.Three theories on the pathogenesis of vitiligo exist: (1) the immune hypothesis, (2) the neuralhypothesis, and (3) the self-destruction hypothesis. Recently, it was suggested that vitiligo is aprimary failure of keratinocytes [7]. Vitiligo is generallyaccepted as an autoimmune disease on the basis of the following evidence: presence ofautoantibodies against melanocytes [8], association of the disease with HLA antigens [9],association of the disease with other autoimmune conditions such as thyroid diseases, adrenalinsufficiency, diabetes mellitus and autoimmune chronic active hepatitis. Autoimmunedestruction of melanocytes may be caused by both cell-mediated and humoral immunity [10].Vitiligo-like lesions also have been reported in 4 patients with melanoma treated with interleukin2 [11].The IFNs have numerous effects on the cells of the immune system by altering cell growth anddifferentiation. In general, the effects of INFs are antiproliferative and induce cellulardifferentiation. The mechanism of action of IFN in the development of vitiligo is not clear. Itmay induce antimelanocyte autoantibodies which destroy normal melanocytes, or it may act aninducing factor for vitiligo by activation of cytotoxic T cells. But the other drugs which wereused in combination with IFN may have had a role in the development of vitiligo in previouscases [5]. A patient with chronic hepatitis C infection developed vitiligo 3 months afterdiscontinuing alpha-INF therapy, and vitiligo was still persistent 6 months after discontinuingtherapy [6]. But in our case vitiligo had disappeared after INF therapy. We conclude thatautoimmune side effects should be closely monitored during IFN therapy of chronic activehepatitis C. KARGERE-Mail [email protected] Fax+ 41 61 306 12 34 http://www.karger.ch.© 1996 S.KargerAG, Basel1 ü 18-8665/96/1931-0065$ 10.00/0ReferencesOrtonne JP, Bose SK: Vitiligo: Where do we stand? Pigment Cell Res 1993;6:61-72.Simsek H: Interferon-alpha treatment of he-modialysis patients with chronic viral hepatitis C andits impact on kidney transplantation. Nephrol Dial Transplant, in press.Primo J, Hinojosu J, Moles JR, Fernandez J, Martinez J, Miralles A, Otte A: Development ofthyroid dysfunction after alpha-interferon treatment of chronic hepatitis C. Am J Gastro-enterol1993;88:1976-1977.García-Lora E, Tercedor J, Massare E, Lopez-Nevot MA, Skiljo M, Garcia-Mellado V: Inter-feron-induced psoriasis in a patient with chronic hepatitis C. Dermatology 1993; 187: 280.Harris J, Bines S, Das Gupta T: Therapy of disseminated metastatic melanoma with re-combinant alpha 2b-interferon and piroxicam: Clinical results with a report of an unusual Downloadedby: 54.70.40.11-11/20/20179:06:03PM response-associated feature (vitiligo), and unusual toxicity (diffuse pulmonary interstitial fi-brosis). Med Pediatr Oncol 1994;22:103-106. Bernstein D, Reddy KR, Jeffers L, Schiff E:Canities and vitiligo complicating interferon therapy for hepatitis C. Am J Gastroenterol1995;90:1176-1177.Schallreuter KU, Lemke R, Brandt O, Schwartz R, Westhoven M, Montz R, Berger J: Vitiligoand other diseases: Coexistence or true association? Dermatology 1994;188:269-275. Naughton GK, Eisinger M, Bystryn JC: Antibodies to normal human melanocytes in vitiligo. JExp Med 1983;158:246-251.Lorini R, Orecchia G, Martinetti M, Dugoujon JM, Cuccia M: Autoimmunity in vitiligo;relationship with HLA, Gin and Km polymorphisms. Autoimmunity 1992;1:255-260. Abdel-Naser MB, Kruger-Krasagakes S, Kra-sagakis K, Gollnick H, Orfanos CE: Furtherevidence for involvement of both cell mediated and humoral immunity in generalized vitiligo.Pigment Cell Res 1994;7:1-8.Wolkenstein P, Chosidow O, Guillaume JC, WechslerJ, Avil MF, RevuzJ: Vitiligo-like lesionsin melanoma treated with interleukin-2: 4 cases. Ann Dermatol Vénéréol 1992; 119: 907-909.Dermatology 1996;193:66-67M.A. Muñoz A.M. Pérez-Bernai EM. CamachoDepartamento de Dermatología M.Q. y Venereología, Hospital Universitario Virgen Macarena,Sevilla, EspañaKey WordsLichenoid eruption Blaschko lines Drug reactions NicergolineLichenoid Drug Eruption Following the Blaschko LinesAbstractEruptions similar to those of lichen planus (LP) are associated with systemic diseases or havebeen induced by many drugs. Linear lesions as a Koebner effect are frequently found in LP butisolated long, narrow, linear lesions, which may extend the whole length of the limb, are rarethough rather more common in childhood. Some cases of zonal or zosteriform LP have beendescribed in the literature. We describe a case of LP with a linear distribution following theBlaschko embryologic lines induced by nicergoline in a 65-year-old woman with a 6-monthhistory of a pruritic eruption of erythematoviolaceous papules on the left breast, trunk and upperlimb, with histological features of LP. It would be the first case of linear LP associated withdrugs. Linear and zosteriform variants of lichen planus (LP) are rare forms of LP. To our knowledgethese forms of LP have not been associated with drugs. We describe a case of LP with a lineardistribution following the Blaschko embryologic lines induced by nicergoline.Case ReportWe observed a 65-year-old woman with a history of hypertension treated with nicergoline, an α-adrenergic blocking agent, for6 months. She presented a pruritic eruption with a linear distribution 4 months after beginningthis treatment. Physical examination revealed an erythematoviolaceous eruption consisting offlat-topped shiny papules along the Blaschko lines affecting the left breast, hemithorax, axillaewith an ‘S’ shape and a longitudinal location on the ventral side of the left arm (fig. 1). Routinelaboratory examination including blood count and hepatic parameters as well as spinal cervical Downloadedby: 54.70.40.11-11/20/20179:06:03PM and dorsal column X-rays were normal. The cutaneous biopsy showed hyperkeratosis withprominent focal hypergranulosis, Civatte bodiesand hydropic degeneration of the basal epidermal layer with Max-Joseph spaces. A lichenoidlymphocytic infiltrate with numerous eosinophils in superficial and mid-dermis was present.Treatment with nicergoline was stopped and 2 months later only a residual lesion on the axillaeremained which was infiltrated with betametasone (3 mg/ml) and 1 month later had completelydisappeared.Lichenoid drug eruption (LDE) may be clinically identical to idiopathic LP and a detailedclinical history is important in order to make the diagnosis [1], Numerous drugs can be inducersof LDE [2] and α-adrenergic KAKGERE-Mail karger¢7⁄8arger.ch Fax+ 41 61 306 12 34 http://www.karger.ch© 1996 S.KargerAG, Basel1018-8665/96/1931-0066$ 10.00/0Miguel A. Muñoz Departamento de Dermatología Hospital Virgen Macarena Avda. Dr. Fedrianis/n E-41075 Sevilla (Spain)Received: October 19. 1995 Accepted: January 26, 1996 Downloadedby: 54.70.40.11-11/20/20179:06:03PM