Previously termed pruritus gravidarum, this condition is found in 0.5 percent of pregnancies (Wikstrom Shemer, 2013). In contrast to the other pregnancy-speciic dermatoses, intrahepatic cholestasis of pregnancy generally has no primary skin lesions. Rarely, a rash precedes pruritus, which is usually associated with abnormally elevated serum bile acid levels and mildly increased hepatic aminotransferase levels (Chao, 2011). Adverse fetal efects have been linked to this condition, and it is discussed in detail in Chapter 55 (p. 1059).
his rare autoimmune bullous disease is notable for its maternal and fetal efects. Initially, pruritic papules and urticarial plaques form and are then followed in most cases after 1 to 2 weeks by vesicles or bullae. Lesions are frequently distributed periumbilically, often develop on other skin surfaces, but spare mucous membranes, scalp, and face (Fig. 62-1).
Previously termed hepes gestationis, pemphigoid gestationis is not related to the herpesvirus. Instead, maternal immunoglobulin G (IgG) antibodies target collagen VII found in the basement membrane of skin and amnionic epithelium (Kelly, 1988; Shimanovich, 2002). Collagen VII is also termed bullous pemphigoid 180 (BP 180). Autoantibody binding to collagen VII activates complement to promote eosinophil chemotaxis to the antigenantibody complexes. Eosinophilic degranulation damages the dermal-epidermal junction and leads to blistering (Engineer, 2000).
In most cases, PG develops during a irst pregnancy. It may rarely be associated with gestational trophoblastic disease (Matsumoto, 2013; Takatsuka, 2012). Most subsequent pregnancies are also afected, usually earlier and more severely (Tani, 2015). Whites have a higher incidence, and other autoimmune diseases are frequent in afected women (Shornick, 1984, 1992).
PG usually begins during the second or third trimester, but postpartum onset or exacerbation is common (Lawley, 1978). The disease course is often marked by antepartum flares and remissions. And, especially in cases with early-onset and blistering, PG has an association with preterm birth and fetalgrowth restriction (Al-Saif, 2016; Chi, 2009). One theory for
TABLE 62-1 . Pregnancy-specific Dermatoses
Cholestasis of Common No primary lesions, secondary Increased perinatal Anti pru ritics, pregnancy excoriations from scratching morbidity cholestyramine, plaques of on abdomen, thighs, buttocks, pregnancy (PUPPP) especially within striae, but
Atopic eruptions of None
Anti pru ritics, Eczema of pregnancy Common Dry, red scaly patches on emollients, topicalextremity flexures, neck, face corticosteroids, oral Prurigo of pregnancy Common 1-5 mm pruritic red papules on steroids if severe extensor surfaces, trunk
Pruritic folliculitis of Rare Small red papules, sterile