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Obstetric cholestasis: current opinions and management
1Department of Obstetrics and Gynaecology, Singapore General Hospital, Outram Road, Singapore 169608.
Obstetric cholestasis (OC) is a pregnancy-specific liver condition that typically presents with generalised pruritus in the absence of a rash in the late second trimester or third trimester. It is more common in certain ethnic groups, particularly those from South Asian, South American, Nordic and Scandinavian regions, and has a familial and genetic basis. Recent research suggests that the pathophysiology may reside in mutations in genes that code for bile acid transporter proteins. Mutations involving the bile acid transporters may impair maternal excretion and influence transplacental passage of bile acids. It is hypothesised that the surge in pregnancy steroid hormones may result in genetically predisposed women developing cholestasis. The condition is also associated with increased perinatal morbidity and mortality, particularly from preterm labour, fetal distress and intrauterine deaths. Animal studies have shown that bile acids are cardiotoxic, which may help explain the condition's association with fetal distress and stillbirths. Accurate diagnosis relies on a high index of suspicion, and the findings of abnormal liver function tests and raised serum bile acid levels after the exclusion of other organic causes of liver disease. Ursodeoxycholic acid helps relieve symptoms, improve serum bile acid levels and possibly has a cardioprotective effect. Active management, in the form of close antepartum fetal monitoring and delivery before 37 weeks, helps to decrease the risk of intrauterine deaths, though possibly at the expense of increased obstetric intervention. Following delivery, there is usually a dramatic improvement of symptoms and resolution of the condition. Women should be counselled about the high recurrence risk of OC in subsequent pregnancies.
Obstetric cholestasis (OC) is a pregnancy-specific liver condition that typically presents with generalised pruritus in the absence of a rash in the late second trimester or third trimester. It is more common in certain ethnic groups, particularly those from South Asian, South American, Nordic and Scandinavian regions, and has a familial and genetic basis. Recent research suggests that the pathophysiology may reside in mutations in genes that code for bile acid transporter proteins. Mutations involving the bile acid transporters may impair maternal excretion and influence transplacental passage of bile acids. It is hypothesised that the surge in pregnancy steroid hormones may result in genetically predisposed women developing cholestasis. The condition is also associated with increased perinatal morbidity and mortality, particularly from preterm labour, fetal distress and intrauterine deaths. Animal studies have shown that bile acids are cardiotoxic, which may help explain the condition's association with fetal distress and stillbirths. Accurate diagnosis relies on a high index of suspicion, and the findings of abnormal liver function tests and raised serum bile acid levels after the exclusion of other organic causes of liver disease. Ursodeoxycholic acid helps relieve symptoms, improve serum bile acid levels and possibly has a cardioprotective effect. Active management, in the form of close antepartum fetal monitoring and delivery before 37 weeks, helps to decrease the risk of intrauterine deaths, though possibly at the expense of increased obstetric intervention. Following delivery, there is usually a dramatic improvement of symptoms and resolution of the condition. Women should be counselled about the high recurrence risk of OC in subsequent pregnancies.
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