Bullous pemphigoid is an acquired blistering disease of the elderly, usually over the age of 60. Multiple medications have been reported to induce bullous pemphigoid, however, only furosemide has been convincingly implicated. Tense bullae form on flexor arms and legs, abdomen, and groin that heal without scarring. In urticarial BP, there are erythe-matous edematous plaques without overt blisters that resemble urticaria and sometimes eczema (Fig. 3A).
■ Subepidermal bulla forms a "clean split" of epidermis from dermis (Figs. 3B-D)
■ Usually no injury to epidermis (no apoptotic keratino-cytes)
■ Eosinophils usually the predominant cells within the blister cavity and in dermis
■ Eosinophils along the basement membrane zone—the key to the diagnosis (Figs. 3C and E)
■ Eosinophilic spongiosis (eosinophils in the epidermis), occasionally
■ In urticarial bullous pemphigoid, no blister seen, but eosinophils tag the basal layer of keratinocytes of spon-giotic epidermis (Fig. 3E) and the papillary dermis is edematous
Mucous membrane pemphigoid; pemphigoid gestationis; epidermolysis bullosa acquisita
■ DIF: linear IgG and third component of complement (C3) at the basement membrane zone of perilesional skin (Fig. 3F). IgG4 predominates.
■ IIF: circulating antibodies to the basement membrane zone of human skin or monkey esophagus in about 70% of patients with bullous pemphigoid
■ IIF-SSS: immunoreactants localized to the epidermal side (roof ) of the blister in 90% of patients (Fig. 3G)
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