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| Pregnancy dermatosis | Suggested pathogenesis | Clinical features | Localisation | Paraclinical diagnosis | Treatment | Fetal concerns |
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| Pemphigoid gestationis (PG) | Complement-fixing IgG antibodies and complement C3 react with the amniotic epithelium of placental tissues and the basement membrane of the skin causing an autoimmune response resulting in tissue damage and blister formation | Pruritic urticarial papules and annular plaques followed by vesicles and finally large tense bullae on an erythematous background | Eruption site is the periumbilical area (most common), rest of the abdomen, thighs, palms, and soles | Histology: urticarial lesions with superficial and deep perivascular lymphohistiocytic eosinophil infiltration
DIF: linear deposition of IgG and C3 complement at the BMZ | Oral corticosteroids at a daily dose of 0.5 mg/kg gradually tapered to a maintenance dose depending on the activity of the disease
Classes III-IV topical steroids.
Cyclosporine A, dapsone, azathioprine, or methotrexate (postpartum) | Passive transfer of IgG1 antibodies can cause mild urticaria-like or vesicular skin lesions in newborns
Risk for premature birth and small-for-gestational-age babies
Risk of small-for-gestational-age and preterm birth with cyclosporine A
Drug toxicity should also be monitored in the mother |
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| Polymorphic eruption of pregnancy (PEP) | Abdominal distension causing subsequent damage to the connective tissue triggering an inflammatory response
Differences in cortisol level in patients with PEP
Connection to atopy | Intensely pruritic urticarial rash with erythematous, edematous papules, and plaques, developing into polymorphic features such as papulovesicles, erythema, and annular wheals | Onset on the abdomen with sparing of the umbilical region as a characteristic finding, which later spreads to thighs, buttocks, and back | Histology: dermal edema with a superficial to mid-dermal perivascular lymphohistiocytic infiltrate composed of eosinophils, Th cells, and macrophages | Topical corticosteroids and oral antihistamines
Oral corticosteroids | No adverse effects related to PEP
Prednisone and prednisolone do not readily cross the placenta and can be safely used during pregnancy
Drug toxicity should be monitored in the mother
Only certain antihistamines approved during pregnancy |
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| Intrahepatic cholestasis of pregnancy (ICP) | Hormonal changes
Genetic predisposition
Exogenous factors (seasonal variability and dietary factors) | Severe pruritus with no primary skin lesions occurring with or without jaundice | Onset on palms and soles to later become generalized
Secondary lesions such as excoriations, scratch marks, and prurigo nodules might develop | Elevated serum bile acid levels (and aminotransferases) | Ursodeoxycholic acid to alleviate the severity of pruritus and to give a more favorable outcome of pregnancy and the absence of adverse events
UVB Phototherapy | Premature birth
Intrapartal fetal distress
Stillbirth
Vitamin K deficiency and coagulopathy in the mother and newborn |
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| Atopic eruption of pregnancy (AEP) | Altered pattern of Th cells with a reduced production of Th1 cytokines (IL-2, interferon gamma, and IL-12) and an increased Th2 cytokine (IL-4 and IL-10) production | Pruritus, prurigo lesions/excoriations, and eczematous-like skin lesions Secondary infection due to excoriations | 66% present with widespread eczematous changes affecting typical atopic sites
33% have small pruritic, erythematous papules on the trunk and limbs | No pathognomonic findings specific to AEP
Elevated serum IgE levels in 20–70% | Topical corticosteroids classes II–IV
Oral corticosteroids and antihistamines
UVB phototherapy
Antibiotics in cases of secondary infection | No adverse effects except the uncertain risk for the child to develop atopic dermatitis |
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