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Linear immunoglobulin A bullous dermatosis: case report A 20-year-old man developed linear immunoglobulin A bullous dermatosis following treatment with piperacillin/tazobactam and doxycycline for leptospirosis, and proton pump inhibitor therapy with omeprazole and pantoprazole [routes and dosages not stated]. The man was admitted with itchy target lesions on his abdomen and arms for 5 days. One month prior to the presentation, he had developed leptospirosis, for which he was admitted and treated with piperacillin/tazobactam, doxycycline, pantoprazole and methylprednisolone for 3 weeks. Thereafter, he was discharged on omeprazole and methylprednisolone for 1 week. However, because of stomach ache due to unknown aetiology, his omeprazole was replaced with pantoprazole. On the next day, he developed skin rash. On current admission, laboratory examinations showed increased serum levels of alanine aminotransferase, bilirubin, lactate dehydrogenase and IgA. The man was then treated with methylprednisolone. Following a 3 day treatment with methylprednisolone, he showed improvement. Subsequently, the man was re-initiated on omeprazole. However, after receiving omeprazole for 2 days, the rash suddenly transformed into generalised blisters. Tense vesicles and blisters filled with serous fluid were noted against an erythematous background on his face, trunk and extremities, and the lesions were distributed symmetrically. Few of the areas had bullous lesions, which were clustered around a resolving lesion and appeared like a "cluster of jewels." Initially, this was considered as an allergy to omeprazole. Therefore, omeprazole therapy was changed to ranitidine. After that, a histopathological examination of a biopsy specimen demonstrated a basket-weave structure of the stratum corneum, necrotic keratinocytes, full-thickness epidermal necrosis, interface change, mild lymphocytic infiltration, colloid bodies, epidermal bullae and sub-epidermal blisters with scattered eosinophils. A marked continuous linear deposition of IgA along the dermal-epidermal junction was observed on direct immunofluorescence. Indirect immunofluorescence test results were negative for IgG or IgA at the dermal-epidermal junction. Also, the results of an enzyme-linked immunosorbent assay for anti-desmoglein 1 and 3 were negative. Based on these findings, a diagnosis of drug-induced linear IgA bullous dermatosis. Therefore, he was treated with immunoglobulin therapy due to the severity and rapid deterioration in his clinical condition. New blisters development decreased over 48 hour following the epithelialisation after the fifth immunoglobulin therapy. After 2 weeks of treatment, complete drying and desquamation of blisters were noted. Han R, et al. Erythema multiforme-like linear immunoglobulin A bullous dermatosis. Indian Journal of Dermatology, Venereology and Leprology 86: 577-580, No. 5, Oct 803517377 2020. Available from: URL: http://doi.org/10.4103/ijdvl.IJDVL_180_19

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