Intrahepatic cholestasis of pregnancy

Intrahepatic cholestasis of pregnancy (ICP) is characterized by maternal pruritus (itch) and liver dysfunction, with raised total serum bile acid concentrations, in the absence of other contributing liver disorders and restricted to pregnancy.

The condition is associated with an increased risk of adverse pregnancy outcomes for the newborn, including spontaneous preterm birth, meconium-stained amniotic fluid, neonatal unit admission, and, if the mother’s serum bile acid concentrations are elevated to a level of ≥100 micromol/L, stillbirth. Maternal complications include an increased risk of gestational diabetes and preeclampsia, in addition to impaired glucose tolerance and dyslipidemia.

The only definitive cure is delivery of the baby.

Pregnant women with total serum bile acid concentrations of <40 micromol/L and mild itching can be offered symptomatic treatment, such as topical emollients and sedating antihistamines. For women with total bile acid concentrations of <100 micromol/L, there is no increased risk of stillbirth compared with the background population, and thus early delivery (before 40 gestational weeks) to prevent stillbirth is not clearly indicated. However, it is important to continue to measure maternal serum bile acid concentrations because they may increase with advancing gestation.

The risk of stillbirth is increased for pregnant women with total serum bile acid concentrations of ≥100 micromol/L, and so delivery should be offered to these women at 35 to 36 gestational weeks.

Treatment with ursodiol does not effectively reduce total serum bile acid concentrations or clearly prevent stillbirth. However, it does cause a marginal improvement in maternal itch, decrease alanine aminotransferase concentrations, and reduce the risk of spontaneous preterm birth in women with serum bile acid concentrations of ≥40 micromol/L.

Intrahepatic cholestasis of pregnancy (ICP) is a disorder characterized by maternal pruritus (itch) and liver dysfunction, in the absence of other contributing liver disorders and restricted to pregnancy. The condition is caused by a combination of hormonal, genetic, and environmental factors.[1]Smith DD, Rood KM. Intrahepatic cholestasis of pregnancy. Clin Obstet Gynecol. 2020 Mar;63(1):134-51. http://www.ncbi.nlm.nih.gov/pubmed/31764000?tool=bestpractice.com

Maternal complications include an increased risk of gestational diabetes and preeclampsia, in addition to impaired glucose tolerance and dyslipidemia; fetal complications include preterm birth, meconium-staining of the amniotic fluid, neonatal unit admission, and, in pregnant women with bile acid concentrations of ≥100 micromol/L, intrauterine fetal death (stillbirth).[2]Ovadia C, Seed PT, Sklavounos A, et al. Association of adverse perinatal outcomes of intrahepatic cholestasis of pregnancy with biochemical markers: results of aggregate and individual patient data meta-analyses. Lancet. 2019 Mar 2;393(10174):899-909. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6396441 http://www.ncbi.nlm.nih.gov/pubmed/30773280?tool=bestpractice.com