Naproxen-induced lichen planus bullosus.

A 46-year-old woman presented with a 2-month history of pruritic, violaceous maculopapular eruption. The lesions had started on her knees and elbows, then gradually spread all over the body. She had been using naproxen for osteoarthritis since 1 month before the beginning of her eruptions. Dermatological examination revealed small, £at-topped, polygonal erythematous and violaceous papules and plaques on her trunk, arms and legs. Two weeks after the ¢rst examination, tense blisters began developing at the sites of pre-existing lesions (F|g. 1). General physical examination was normal. The patient had been diagnosed as having breast carcinoma 9 years previously. She had then undergone total mastectomy, chemotherapy and radiation therapy. The result of laboratory tests, including urinalysis, complete blood cell count, biochemical analysis, AFP, CEA, CA-125, X-ray examination of the lung, ultrasonographic examination of abdomen, computerized tomography of the abdomen-chest and cranium, were normal. Erythrocyte sedimentation rate was 54 mm/h. Hepatitis markers and serological syphilis reactions were negative. No casual or other provocative factors were detected other than naproxen. A biopsy from 1 of the bullous lesions, which arose on an erythematous lesion, was taken. Hematoxylin-eosin staining showed compact orthokeratosis, epidermal hyperplasia, focal hypergranulosis, vacuolar degeneration of the basal layer, subepidermal vesicle formation and dense band-like in¢ltration of mononuclear in£ammatory cells in the upper dermis. Direct immuno£uorescence studies showed granular deposition of IgG, IgA, IgM and ¢brinogen at the basement membrane zone. Naproxen administration was stopped. She was then treated with topical corticosteroid and the lesions gradually disappeared. After the cessation of therapy, she was followed-up regularly (at 3, 6, 9 and 12 months) with no evidence of relapse.