Which histopathologic features are typical of bullous pemphigoid?

Which histopathologic features are typical of bullous pemphigoid?

• A. Subepidermal blisters with linear IgG/C3 along basement membrane
• B. Suprabasal acantholysis
• C. Full-thickness epidermal necrosis
• D. Intraepidermal edema with spongiosis

Answer: (A)

Bullous pemphigoid is an autoimmune blistering disease where antibodies target components of the basement membrane zone, especially hemidesmosomes. This causes separation right below the epidermis, producing subepidermal blisters. A key histologic picture is a relatively intact epidermis sitting on a dermal inflammatory infiltrate rich in eosinophils, with the blister roof formed by the overlying epidermis. Direct immunofluorescence adds the hallmark: a smooth, continuous line of IgG (and often C3) along the basement membrane. This matches the described pattern: blisters forming beneath the epidermis (subepidermal) and linear deposition of IgG and complement at the dermal-epidermal junction. In contrast, other patterns point to different diseases—for example, suprabasal acantholysis seen in pemphigus vulgaris involves the epidermal layers, not a subepidermal split; full-thickness epidermal necrosis occurs in severe reactions like toxic epidermal necrolysis; and intraepidermal edema with spongiosis is typical of eczematous or inflammatory dermatoses, not BP.

Bullous pemphigoid is an autoimmune blistering disease where antibodies target components of the basement membrane zone, especially hemidesmosomes. This causes separation right below the epidermis, producing subepidermal blisters. A key histologic picture is a relatively intact epidermis sitting on a dermal inflammatory infiltrate rich in eosinophils, with the blister roof formed by the overlying epidermis. Direct immunofluorescence adds the hallmark: a smooth, continuous line of IgG (and often C3) along the basement membrane.

This matches the described pattern: blisters forming beneath the epidermis (subepidermal) and linear deposition of IgG and complement at the dermal-epidermal junction. In contrast, other patterns point to different diseases—for example, suprabasal acantholysis seen in pemphigus vulgaris involves the epidermal layers, not a subepidermal split; full-thickness epidermal necrosis occurs in severe reactions like toxic epidermal necrolysis; and intraepidermal edema with spongiosis is typical of eczematous or inflammatory dermatoses, not BP.