Linear IgA bullous dermatosis is an autoantibody-mediated subepidermal blistering disease that is rarely associated with drug exposure [1]. Clinical differentiation of this entity from more common blistering disorders such as bullous pemphigoid may not be possible on clinical grounds. It has been described in association with many medications [2-5], and vancomycin has been implicated in several patients [4, 5]. We describe two patients with severe linear IgA bullous dermatosis who received vancomycin within 2 weeks before the development of bullae.

A 60-year-old woman had surgical repair of an infected enterocutaneous fistula. Ten days after beginning postoperative intravenous antibiotic therapy with vancomycin, imipenim, and gentamicin, the patient developed widespread bullae (Figure 2, top). Histopathologic examination revealed a subepidermal blister with numerous neutrophils, and direct immunofluorescence revealed linear deposits of IgA along the dermal-epidermal junction; these findings were consistent with drug-induced LABD. Antibiotic therapy was discontinued; therapy with oral prednisone, 60 mg/d, was begun; and the blisters resolved.

View larger version (81K): [in this window] [in a new window]   Figure 2. Linear IgA bullous dermatosis associated with vancomycin. Top. Large tense bullae on the hands of patient 1. Bottom. Tense blisters and erosions, some in an arcuate distribution, on patient 2.

A 71-year-old woman, hospitalized for evolving pneumonia, received one dose of intravenous vancomycin followed by a course of nafcillin. Eight days after antibiotic therapy began, widespread vesicles and bullae developed (Figure 2, bottom). Findings on histopathologic evaluation and direct immunofluorescence were consistent with drug-induced LABD. Therapy with oral prednisone, 60 mg/d, was begun; antibiotic therapy was discontinued; and the bullae resolved. Subsequently, the patient inadvertently received a dose of vancomycin, and the blisters briefly recurred.

Linear IgA bullous dermatosis is a blistering disorder characterized by tense blisters that are filled with neutrophils and are often distributed annularly; the linear deposition of IgA occurs at the dermal-epidermal junction. Although this disorder is usually idiopathic [1], an increasing number of LABD cases associated with exposure to drugs, most often vancomycin, have been reported in the dermatology literature [2-5]. Although the patients in this report received other drugs, we suspect vancomycin as the inciting agent.

Bullous eruptions such as bullous pemphigoid are not uncommon and may be seen in hospitalized patients. However, the abrupt onset of blisters within 1 or 2 weeks of the administration of new medications should arouse suspicion of a drug-induced blistering eruption such as bullous forms of erythema multiforme or drug-induced LABD. Histopathologic findings and direct immunofluorescence aid in differentiating the type of blistering eruption; this better enables identification and discontinuation of therapy with the most likely offending agents.