Diphenylcyclopropenone-Induced Vitiligo in a Patient with Alopecia Universalis
نویسندگان
چکیده
Alopecia areata and vitiligo are autoimmune diseases, both associated with multiple autoimmune comorbidities. Many studies show colocalization of these diseases at the same anatomical site. Here, we have a case where both disorders were reported to present in the same patient. Diphenylcyclopropenone (diphencyprone, DCP) is used in the treatment of alopecia areata and may induce vitiligo in some patients. We report on one case of vitiligo that was induced by DCP during therapy for alopecia universalis. Alopecia areata and vitiligo share many susceptibility genes. Follicular melanocyte destruction may represent the link between the two diseases.
منابع مشابه
Narrow-band ultraviolet B treatment for diphenylcyclopropenone-induced vitiliginous lesions.
Topical immunotherapy, defined as the induction and periodic elicitation of an allergic contact dermatitis by topical application of potent contact allergens, has been used to treat conditions such as alopecia areata (AA) and recalcitrant warts since the 1970s (1). Topical immunotherapy with diphenylcyclopropenone (DPCP) is a safe and sometimes effective treatment for chronic extensive AA and v...
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Diphencyprone (DCP) is a contact sensitizer which is used to treat dermatological disorders with an immunological origin, such as extensive alopecia areata (AA). Vitiligo is a rare but known side effect of DPCP therapy which is formed in the treatment site or remote areas. In this paper a 37-year-old man developed alopecia totalis with loss of eyebrows and eyelashes who presented some vitiligo ...
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Diphenylcyclopropenone (DPCP) is widely considered the most effective topical immunotherapy for refractory or extensive alopecia areata (AA), but questions regarding how long to try DPCP therapy before terminating and what factors are prognostic of therapeutic success still remain unanswered. In this retrospective study of 50 AA patients, we evaluated DPCP efficacy and identified patient factor...
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