Intraheptic 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 afte
r delivery. It recurs in 40-60% of future pregnancies. The intensity o
f pruritus and the laboratory alterations (increased serum bile salts
and transaminases in almost all patients, hyperbilirubinaemia in 20% o
f 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 f
oetal distress, causing premature deliveries and stillbirths. Cholesta
sis of pregnancy has been recognized in most countries and ethnic grou
ps but its prevalence is higher in Chile (14% of deliveries in 1975 an
d approximately 4% in 1995) and in Sweden than in other countries. The
cause is unknown. Sex hormones, mainly oestrogens and progesterone, a
ppear to be involved in its pathogenesis. An interplay between a genet
ic metabolic predisposition and some environmental factor(s) is appare
ntly relevant. Clinical and experimental studies suggest that a margin
al selenium deficiency could be a dietary pathogenic factor. Some drug
s attenuate pruritus and improve maternal cholestasis, but not the foe
tal prognosis. Ursodeoxycholic acid (UDCA) administration provides a s
ignificant improvement in maternal pruritus and in the biochemical abn
ormalities, with no adverse effects in the mother or child. Recent cli
nical and experimental studies show that UDCA administration improves
maternal disease and foetal prognosis without any detectable adverse e
ffects.