Bullous pemphigoid

Bullous pemphigoid typically occurs in older people and has a distinctive clinical appearance. There are several clinical variants, one of which occurs in childhood.

In the prodromal, nonbullous phase, pruritus of variable intensity may be accompanied by eczematous or urticarial lesions for weeks or months.

In the bullous stage, characteristic, tense vesicles or bullae develop on apparently normal or erythematous skin of the pre-existing eczematous or urticarial eruption. If the blisters burst, the eroded, crusty areas slowly heal to leave postinflammatory hyperpigmentation.

The lesions are usually symmetric and favor the flexural aspects of the extremities, lower trunk, and abdomen.

The treatment goal is to decrease or stop blister formation, to promote healing of existing blisters and erosions, and to control the associated pruritus. Topical and systemic corticosteroids, as well as other immunosuppressive and anti-inflammatory agents, are used.

Bullous pemphigoid is a chronic, acquired autoimmune blistering disease characterized by autoantibodies against hemidesmosomal antigens, resulting in the formation of a subepidermal blister.[1]Liu Z. Are anti-BP180 IgG1 or IgG4 autoantibodies pathogenic? J Invest Dermatol. 2002;119:989-990.