Bullous pemphigoid pathology

Bullous pemphigoid is the most common autoimmune skin disease presenting with time crops pruritus blisters, often in older adults. Mucous membrane involvement may occur and there are several clinical subtypes. Autoantibodies target the components of the basement membrane, particularly the BP antigens BP180 and BP230.

Histology bullous pemphigoid

Early injuries during urticarial phase may be nonspecific and show a slight upper part dermal edema with perivascular infiltrate (Figure 1). Often there are conspicuous eosinophils. Immunofluorescence It is very useful in this early phase.

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

Special studies of bullous pemphigoid

Direct immunofluorescence sample linear statement IgG (most frequent IgG4 subtype) and C3 along the basement membrane (Figure 4). Indirect split skin immunofluorescence studies are generally not required, but may be useful in rare cases when aquisite epidermolysis bullosa is suspected.

Differential diagnosis bullous pemphigoid

Dermatitis herpetiform Neutrophils papillary dermal microabscesses seen in dermatitis herpetiformis, it is not usually present in bullous pemphigoid, but it can be present in some variants. Direct immunofluorescence shows granular deposition of IgA.

Linear IgA disease: formation of subepidermal blisters with IgA deposition of linear basement membrane in direct immunofluorescence.

Epidermolysis bullosa aquisita shows subepidermal bullas with linear IgG / C3 deposition, however, indirect immunofluorescence in these conditions reveals positivity in the divided skin floor, whereas bullous pemphigoid has positivity in the epidermal side.

Other causes of subepidermal blisters include epidermolysis bullosa, porphyria delays cutanea, and amyloidosis bullosa.