Table 2.

Diagnostic features of, treatments for, and outcomes with pregnancy-specific dermatoses

Disease	Clinical and diagnostic features	Treatment	Prognosis	Fetal risk
AEP	Eczematous, papular and prurigo skin lesions	First line: emollient therapy Second line: topical GCS and systemic antihistamines Third line: narrowband UVB therapy Fourth line: prednisolone, cyclosporine, azathioprine	Possible recurrence in subsequent pregnancies	Fetal prognosis is unaffected
PEP	Polymorphic skin lesions (urticarial papules that coalesce into plaques, vesicles, widespread erythema, targetoid and eczematous lesions); periumbilical region generally unaffected; never bullae	First line: emollient therapy, topical GCS and systemic antihistamines Second line: systemic prednisolone	Rash usually resolves in 4–6 weeks independent of delivery; disease tends not to recur	Fetal prognosis is unaffected
PG	Begins with pruritus, followed by skin lesions (urticarial papule and bullae); periumbilical region affected DIF: linear IgG/C3 deposition at the basal membrane ELISA: IgG antibodies against BP180	First line: emollient therapy, topical potent GCS and systemic antihistamines Second line: systemic prednisolone Third line: azathioprine, intravenous immunoglobulins, dapsone	Recurrences in subsequent pregnancies are common; long-term increased risk of Graves’s disease	Preterm birth, low birthweight
ICP	Classical triad: (1) pruritus; (2) jaundice (1–4 weeks after pruritus); (3) bile acids elevated (> 10 μmol/l)	Ursodeoxycholic acid (15 mg/kg/day); induced preterm delivery	Resolves spontaneously within 6 weeks after birth	High risk of preterm birth/stillbirth (up to 60%)

AEP atopic eruption of pregnancy, BP180 bullous pemphigoid antigen 180, DIF direct immunofluorescence, ELISA enzyme-linked immunosorbent assay, GCS glucocorticosteroids, ICP intrahepatic cholestasis in pregnancy, IgG immunoglobulin G, PEP polymorphic eruption of pregnancy, PG pemphigoid gestationis, UVB ultraviolet B