Linear IgA bullous dermatosis (LABD) is an uncommon autoimmune subepidermal blistering disorder characterized by deposition of IgA autoantibodies in a lincar pattern along the epidermal basement membrane zone [1, 2]. Most cases of LABD are idiopathic, but an association with vancomycin has been recently described [3]. This association is not yet widely appreciated.

A 65-year-old woman was admitted to the hospital with subarachnoid hemorrhage secondary to a ruptured aneurysm. On hospital day 6, her clinical course was complicated by Pseudomonas aeruginosa and Staphylococcus epidermidis sepsis, for which intravenous vancomycin, gentamicin, and ticarcillin-clavulanate were administered. Other medications included ranitidine, nitroglycerin, nimodipine, ferrous sulfate, and phenytoin. On hospital day 13, confluent erythematous-based vesicobullae developed on the abdomen and proximal extremities (Figure 1, top). No mucosal or palmoplantar involvement was noted. The serum vancomycin trough level was 5.2 µg/mL (normal, 5-10 µg/mL). Skin histopathology revealed subepidermal separation with neutrophils. Direct immunofluorescence evaluation of perilesional skin showed intense linear IgA deposition along the epidermal basement membrane zone. After the biopsy specimen was split by incubation with 2 mmol of NaCl per L [2], the linear IgA deposition localized exclusively on the dermal side of the separation (Figure 1, bottom). Indirect immunofluorescence evaluation of serum detected no circulating anti-basement membrane zone antibodies. Vancomycin therapy was suspected to have caused the blistering eruption and was discontinued. No new skin lesions had developed 2 days after discontinuation of therapy, and rash had completely resolved by hospital day 30. No cutaneous lesions were noticed at 6-month follow-up.

View larger version (90K): [in this window] [in a new window]   Figure 1. Vancomycin-induced linear IgA bullous dermatosis. Top. Extensive and confluent ruptured erythematous vesicles and bullae on the right thigh. Bottom. Direct immunofluorescence evaluation of perilesional skin biopsy specimen.

Vancomycin-induced LABD is defined by a blistering eruption that develops after exposure to intravenous vancomycin, resolves with withdrawal of the drug, and is accompanied by linear IgA deposition in affected skin. This adverse reaction to vancomycin is idiosyncratic, is not associated with specific morbid conditions or excessive serum vancomycin trough levels, and has not occurred after use of oral vancomycin. The delay between first exposure to the drug and the onset of the eruption ranges from 1 to 15 days [3-5]. Drug rechallenge reproduces the disease with a more rapid and severe onset [3-5]. Use of prednisone or dapsone to control blistering is rarely required. The antigen recognized by the IgA autoantibodies is unknown. Vancomycin-induced LABD should be considered in the differential diagnosis of blistering mucocutaneous eruption in patients receiving intravenous vancomycin, and early diagnosis through direct immunofluorescence examination of skin is encouraged.