Bullous pemphigoid is a blistering skin disease in which autoantibodies develop to hemidesmosomal components of the epidermal basement membrane zone, including 2 major antigenic proteins, the 230-kD antigen (BPAG1) and the 180-kD antigen (BPAG2).
1 Bullous pemphigoid has been reported to be medication induced in some cases.
3 Most notably, in a case-control study of the medication history of consecutive patients with bullous pemphigoid compared with that of control patients, a statistically significant OR was found in the association of previous loop diuretic use and bullous pemphigoid.
3 However, the mechanism through which the disease is induced is not well understood. A proposed mechanism suggests that the inducing drug may act as a hapten, altering the antigenicity of the lamina lucida or attaching to a cell site and eliciting the formation of autoantibodies.
8 Additionally, eosinophils have been found to produce and release 92-kD gelatinase, which then cleaves the extracellular, collagenous domain of recombinant 180-kD bullous pemphigoid autoantigen, thereby contributing significantly to the tissue damage in bullous pemphigoid.
9 This process may also play a role in drug-induced bullous pemphigoid because eosinophils are a prominent part of many drug reactions. A few case-control studies have found that patients with bullous pemphigoid are more likely to have various neurologic diseases, schizophrenia, psoriasis, cerebrovascular disease, and dementia before the diagnosis of bullous pemphigoid is made.
6,7 The patient in the current case had a previous diagnosis of a seizure disorder, which is consistent with this finding.