Under the surface: Understanding and managing bullous pemphigoid

Bulous pemphigoid (BP) is the most common autoimmune subepidermal blistering disease in Western populations, and typically occurs in the elderly. Immunologically, BP is characterized by both tissue-bound and circulating autoantibodies against the BP antigen 180 (also referred to as BPAG2), BP antigen 230 (also referred to as BPAG1e), or both. These antigens are components of hemidesmosomes that are involved in dermal–epidermal adhesion. The following are risk factors for BP: advanced age, dementia, Parkinson's disease, cerebrovascular illness, and some medications, such as spironolactone, loop diuretics, and neuroleptics. In the early stages of the disease or in atypical, non-bullous variations, only excoriated, eczematous, or urticarial lesions are seen. Strong topical corticosteroids being an effective first-line treatment for BP, there is ongoing debate regarding their long-term viability. Future substitutes for traditional immunosuppressive medications for maintenance therapy include more recent therapeutic medicines that target molecules implicated in the inflammatory cascade linked to BP.