Abstract

We report a unique case of vancomycin-induced linear IgA bullous dermatosis (LABD) presenting as erythroderma. Direct immunofluorescence showed a linear IgA deposition at the dermal side of the basement membrane zone (BMZ), and double immunostaining using patients’ skin as a substrate revealed that the in vivo IgA signal co-localized with laminin-332 and type VII collagen. Our case is the first documentation of vancomycin-induced LABD, in which the pathogenic IgA deposit would concomitantly recognize the two distinct antigens at the dermal BMZ.

Highlights

  • Linear IgA bullous dermatosis (LABD) is a rare autoimmune subepidermal bullous disease characterized by linear IgA deposition at the basement membrane zone (BMZ), and often shows considerably variable clinical presentation

  • Vancomycin hydrochloride, a glycopeptide antibiotic agent, has frequently been reported [1,2,3,4,5,6], and the rare clinicopathology of the drug-induced LABD can be a noteworthy updating to assist the awareness of the underlying disease cause

  • We report the first case of vancomycin-induced LABD presenting as erythroderma, whose in vivo IgA deposit reacted with both laminin-332 and type VII collagen

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Summary

Introduction

Linear IgA bullous dermatosis (LABD) is a rare autoimmune subepidermal bullous disease characterized by linear IgA deposition at the basement membrane zone (BMZ), and often shows considerably variable clinical presentation. Vancomycin hydrochloride, a glycopeptide antibiotic agent, has frequently been reported [1,2,3,4,5,6], and the rare clinicopathology of the drug-induced LABD can be a noteworthy updating to assist the awareness of the underlying disease cause. We report the first case of vancomycin-induced LABD presenting as erythroderma, whose in vivo IgA deposit reacted with both laminin-332 and type VII collagen.

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