Pregnancy Dermatoses

• Relatively common disorder (~1 in 160 deliveries) that begins late in the third trimester or during the immediate postpartum period; occurs primarily in primiparous women, with an increased frequency in those with multigestational pregnancies.

• Pruritic edematous papules and plaques, whose color varies from pink to red-brown depending on skin phototype, that often involve the abdominal striae but spare the umbilicus (Fig. 22.1); polymorphic presentation includes patches of erythema, targetoid lesions, tiny vesicles, and eczematous plaques (Fig. 22.2).

• Lesions can become widespread, but usually spare the face, palms, and soles; the eruption spontaneously resolves within 4–6 weeks after delivery.

• In general, does not recur with subsequent pregnancies, in contrast to pemphigoid gestationis (PG), and there is no fetal risk.

• DDx: PG (may require direct immuno­fluorescence [DIF] of perilesional skin to distinguish), urticarial drug eruption, viral exanthem, allergic contact dermatitis, scabies, erythema multiforme minor.

• Rx: topical CS and oral antihistamines usually suffice (see Appendix); occasionally, severe cases require oral CS (prednisolone preferred during pregnancy because of significant inactivation by placenta, leading to a mother : fetus ratio of 10 : 1).

• Unusual pruritic vesiculobullous disorder with significant clinical and histologic overlap with bullous pemphigoid (see Chapter 24).

• Usually develops during the later stages of pregnancy or immediately postpartum and is due to circulating autoantibodies against bullous pemphigoid antigen 180 (BP180) present within the hemidesmosome of the basement membrane zone (BMZ).

• In theory, it is related to aberrant expression of MHC class II antigens of paternal origin in the placenta that trigger an autoimmune response to the placental BMZ, followed by cross-reactivity with the BMZ of the skin.

• Lesions often begin on the abdomen, including around and within the umbilicus, but then become more widespread on the trunk as well as the extremities; in addition to vesicles and bullae, edematous urticarial plaques are seen (Fig. 22.3).

• DIF of perilesional skin shows linear deposits of C3 at the BMZ.

• Increased risk of small-for-gestational age and premature neonates and ~10% of newborns have mild skin involvement; often flares at the time of delivery and recurs during subsequent pregnancies.

• DDx: primarily PEP (but in PEP, patients are usually primiparous, large bullae are rare unless there is marked background edema, lesions spare the umbilicus, and DIF of perilesional skin is negative) (Fig. 22.4); urticarial drug eruption, allergic contact dermatitis.

• Rx: potent topical or oral CS (prednisolone 0.5 mg/kg/day; see Appendix), depending on severity.

• Pruritic papules and eczematous plaques that usually develop earlier during pregnancy than other disorders described in this chapter (Fig. 22.5).

• Patients have an atopic diathesis, but the eruption is more likely to have its initial presentation during pregnancy and less often it represents a flare of pre-existing atopic dermatitis.

• May be explained by the predominance of a Th2 immune response during pregnancy.

• No maternal or fetal risks, but recurrence during subsequent pregnancies common.

• DDx: PEP, intrahepatic cholestasis of pregnancy, scabies, allergic contact dermatitis, drug eruption or viral exanthem (if papular).

• Rx: topical CS, oral antihistamines, and other routine therapies for atopic dermatitis (e.g. emollients; oral antibiotics such as cephalexin if secondary bacterial infection; see Chapter 10); NBUVB phototherapy or oral CS for more severe cases.

• Onset usually during the third trimester, related in part to peak in estrogen levels; genetic predisposition with higher incidence in native South Americans; hepatitis C viral infection is also a risk factor.

• Cholestasis leads to elevated serum levels of bile acids and this leads to intense pruritus.

• Cutaneous lesions are nonspecific and vary from excoriations to prurigo nodularis (Fig. 22.6); jaundice occurs in a small minority of patients.

• Important to diagnose because cholestasis of pregnancy is associated with intrapartum fetal distress, prematurity, and stillbirths; in severe cases, vitamin K deficiency may occur, with an increased risk of hemorrhage.

• Diagnosis is based on measurement of total serum bile acids, with elevations typically ranging from 3 to 100 times normal.

• DDx: other causes of cholestasis (e.g. primary biliary cirrhosis) and hepatitis (e.g. hepatitis B, hepatitis C), especially if pruritus does not resolve within days of delivery; scabies, atopic eruption of pregnancy other causes of primary pruritus (see Fig. 4.1).

• Rx: oral ursodeoxycholic acid (15 mg/kg/daily or 1 g daily); if elevated prothrombin time, vitamin K injections; alert patient that disorder recurs in at least 50% of subsequent pregnancies.