Abstract and Introduction
Bullous pemphigoid (BP), usually seen in the elderly, is the most common autoimmune blistering disease. The various clinical presentations of BP, similar and associated diseases, and the pathophysiology of autoantibodies of the IgG class, which target hemidesmosomal proteins causing a dermalepidermal split, are discussed. Treatment regimens can vary, and the common standard treatment combinations are described.
Bullous pemphigoid (BP) is an autoimmune disease characterized by subepidermal blistering most often affecting the elderly, but can also present in younger patients, equally affecting males and females (Fitzpatrick et al., 2008). Studies indicate an annual incidence between 0.2 and 3 per 100,000 persons (Langan et al., 2008). The severity of BP varies between patients and among individual patients over time. Treatment regimens often require alterations according to the severity of the disease and the side effects of drugs (Patton & Korman, 2006). BP initially presents as urticarial lesions and may take weeks to months to erupt into bullae (Fitzpatrick et al., 2008). The initial eruptions are usually localized and then may progress to a generalized appearance. Histopathological assays upon direct immunofluorescence testing show immunoglobulin G (IgG) autoantibodies deposited at the epidermal basement membrane, which target two hemidesmosomal proteins of 230 kD and a 180 kD. C3 is found along the basement membrane zone of epidermal layers (Chan, 2008; Fitzpatrick et al., 2008) assays also show infiltration of neutrophils and eosinophis in the dermis (Fitzpatrick et al., 2008). Circulating IgG are characteristic upon indirect immunoflourescent examination (Fitzpatrick et al., 2008).
Dermatology Nursing. 2009;21(6):322-326. © 2009 Jannetti Publications, Inc.
Cite this: Bullous Pemphigoid: A Short Review - Medscape - Nov 01, 2009.