Intrahepatic cholestasis of pregnancy is characterized by skin
pruritus and a biochemical
cholestasis of mild to moderate severity appearing during pregnancy (mainly in the third trimester) and disappearing after delivery. It recurs in 40-60% of future pregnancies. The intensity of
pruritus and the laboratory alterations (increased serum
bile salts and
transaminases in almost all patients, hyperbilirubinaemia in 20% of patients) fluctuate during one pregnancy and also vary in subsequent affected pregnancies. This disease has no meaningful consequences for the mother; in contrast, it is associated with an increased risk of foetal distress, causing premature deliveries and
stillbirths.
Cholestasis of pregnancy has been recognized in most countries and ethnic groups but its prevalence is higher in Chile (14% of deliveries in 1975 and approximately 4% in 1995) and in Sweden than in other countries. The cause in unknown.
Sex hormones, mainly oestrogens and
progesterone, appear to be involved in its pathogenesis. An interplay between a genetic metabolic predisposition and some environmental factor(s) is apparently relevant. Clinical and experimental studies suggest that a marginal
selenium deficiency could be a dietary pathogenic factor. Some drugs attenuate
pruritus and improve maternal
cholestasis, but not the foetal prognosis.
Ursodeoxycholic acid (UDCA) administration provides a significant improvement in maternal
pruritus and in the biochemical abnormalities, with no adverse effects in the mother or child. Recent clinical and experimental studies show that UDCA administration improves maternal disease and foetal prognosis without any detectable adverse effects.