Drug-induced cicatricial pemphigoid and acquired epidermolysis bullosa.

A utoimmune diseases probably have a multitude of causes. It is obvious that exogenous agents, particularly drugs, may trigger the development of autoimmune responses leading to bullous eruptions. In the literature several cases of drug-induced (disseminated) bullous pemphigoid (BP) have been reported (see article by Fellner in this issue); however, localized variants of pemphigoid and acquired epidermolysis bullosa, although to a lesser extent, apparently can also be induced by drugs. Important localized variants of pemphigoid are cicatricial pemphigoid (Cl’) (synonyms: mucous membrane pemphigoid [MMP], ocular pemphigoid) and two nonmucosal localized variants: the non-mucosal scarring type pemphigoid (Brunsting-Perry type) and the nonscarring localized-type pemphigoid (LBP). Cicatricial pemphigoid is a rather rare disease of late middle age that occurs particularly on the mucous membranes of the eyes, oropharynx, genitalia, or anus. The characteristic skin picture is that of localized recurrent blisters with the development of scarring.’ The cicatricial process can cause serious adhesions, strictures, and depending on the localization, on the long-term loss of function. Histologically, in contrast to BP, eosinophils in LBP and CP are usually present in significantly small numbers. Particularly in Cl’ lesions, a fairly dense, sometimes predominant lymphocytic inflammatory infiltrate is observed in the dermis. Immunofluorescence (IF) studies in CP show a linear deposition of IgG and complement along the basement