Pathology of Bullous Pemphigoid

Bullous pemphigoid is the most common defect dermatosis presenting time-course edema blisters, often in older adults. Mucosal Mucosal involvement can occur and several clinical subtypes exist. Autoantibodies are directed against the components of the basement membrane, particularly the BP antigens BP180 and BP230.

Histology of bullous pemphigoid

Early lesions during the hives phase may be nonspecific and show mild upper dermal dermal edema with perivascular infiltrate (Figure 1). Eosinophils are often conspicuous eosinophils. Immunofluorescence is very useful in this initial phase.

Established blister: the blister is edema and contains fibrin and a large number of inflammatory cells including eosinophils (Figures 2, 3). Eosinophils can be very dense in areas and form small abscesses in the superficial dermis.

Special studies of bullous pemphigoid

Direct immunofluorescence specimens linear assessed of IgG (most often IgG4 subtype) and C3 along the basement membrane (Figure 4). Indirect immunofluorescence studies of split skin are generally not necessary but can be useful in rare cases when epidermolysis bullosa acquisita is suspected.

Differential Diagnosis of bullous pemphigoid

Dermatitis herpetiformis: Neutrophils dermal papillary microabscesses that are seen in dermatitis herpetiformis are usually not present in bullous pemphigoid, but may be present in some variants. Direct immunofluorescence specimens granulomatous of IgA deposition.

Linear IgA disease: subepidermal blister formation with linear IgA deposition at the basement membrane by direct immunofluorescence.

Epidermolysis bullosa acquisita shows subepidermal bullae with linear IgG/C3 deposition; however, indirect immunofluorescence in these conditions reveals positivity on the floor of the split skin, whereas bullous pemphigoid has positivity on the epidermal epidermal side.

Other causes of subepidermal blisters include epidermolysis bullosa, is suspected. cutanea tarda, and bullous amyloidosis.