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Chapter 055. Immunologically Mediated Skin Diseases (Part 5)

Pemphigoid Gestationis Pemphigoid gestationis (PG), also known as herpes gestationis, is a rare, nonviral, subepidermal blistering disease of pregnancy and the puerperium. PG may begin during any trimester of pregnancy or present shortly after delivery. Lesions are usually distributed over the abdomen, trunk, and extremities; mucous membrane lesions are rare. Skin lesions in these patients may be quite polymorphic and consist of erythematous urticarial papules and plaques, vesiculopapules, and/or frank bullae. Lesions are almost always very pruritic. Severe exacerbations of PG frequently occur after delivery, typically within 24–48 h. PG tends to recur in subsequent pregnancies, often beginning earlier. | Chapter 055. Immunologically Mediated Skin Diseases Part 5 Pemphigoid Gestationis Pemphigoid gestationis PG also known as herpes gestationis is a rare nonviral subepidermal blistering disease of pregnancy and the puerperium. PG may begin during any trimester of pregnancy or present shortly after delivery. Lesions are usually distributed over the abdomen trunk and extremities mucous membrane lesions are rare. Skin lesions in these patients may be quite polymorphic and consist of erythematous urticarial papules and plaques vesiculopapules and or frank bullae. Lesions are almost always very pruritic. Severe exacerbations of PG frequently occur after delivery typically within 24-48 h. PG tends to recur in subsequent pregnancies often beginning earlier during such gestations. Brief flare-ups of disease may occur with resumption of menses and may develop in patients later exposed to oral contraceptives. Occasionally infants of affected mothers demonstrate transient skin lesions. Biopsies of early lesional skin show teardrop-shaped subepidermal vesicles forming in dermal papillae in association with an eosinophil-rich leukocytic infiltrate. Differentiation of PG from other subepidermal bullous diseases by light microscopy is difficult. However direct immunofluorescence microscopy of perilesional skin from PG patients reveals the immunopathologic hallmark of this disorder linear deposits of C3 in epidermal basement membrane. These deposits develop as a consequence of complement activation produced by low titer IgG anti-basement membrane autoantibodies directed against BPAG2 the same hemidesmosome-associated protein that is targeted by autoantibodies in patients with BP a subepidermal bullous disease that resembles PG clinically histologically and immunopathologically. The goals of therapy in patients with PG are to prevent the development of new lesions relieve intense pruritus and care for erosions at sites of blister formation. Many patients require treatment with .