Intrahepatic Cholestasis of Pregnancy: A Narrative Review

Abstract

This narrative review synthesizes the current literature on the pathogenesis and management of Intrahepatic Cholestasis of Pregnancy (ICP). ICP is a multifactorial liver disorder characterized by intense pruritus and elevated serum bile acids (SBA) and/or liver enzyme levels, typically emerging in the second or third trimester and resolving postpartum. Its etiology involves a complex interplay of genetic factors, hormonal influences (e.g., elevated estrogen and progesterone levels), and environmental factors, supported by varied global prevalence (9.2–15.6% in South America vs. 0.1–0.5% in Europe) and high recurrence rates (45–90%). Diagnosis requires the exclusion of other hepatobiliary diseases and the presence of pruritus with a random peak SBA concentration ≥10 μmol/L (or ≥19 μmol/L, depending on the specific guideline used).

Ursodeoxycholic acid (UDCA) (10–20 mg/kg/day) is the first-line treatment, reducing maternal symptoms and transaminase levels, though its effect on stillbirth is debated. Vitamin K supplementation is advised for a prolonged prothrombin time. Antenatal surveillance includes monitoring liver function and SBA every 1–2 weeks. Fetal monitoring, while necessary, has limited predictive value for sudden fetal death. The risk of stillbirth correlates strongly with SBA levels (3.44% for ≥100 μmol/L).

Management focuses on risk-stratified delivery timing: ≥100 μmol/L warrants delivery at 35–37 weeks; 40–99 μmol/L suggests 37 weeks; and <40 μmol/L may continue to 39 weeks. Postpartum, SBA, and liver function should be reassessed at 6–8 weeks.