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Severe Obstetric Cholestasis

Key points

  • Severe obstetric cholestasis is associated with an increased risk of adverse fetal outcomes.
  • The risk of adverse fetal outcomes is thought to be increased in women with severe obstetric cholestasis.
  • There are no prospective national studies to estimate the incidence or outcomes of severe obstetric cholestasis in pregnancy.
  • This study will investigate the incidence, management and outcomes for mother and infant in pregnancies where the mother has severe obstetric cholestasis.

Surveillance Period

June 2010- May 2011


Severe obstetric cholestasis (OC), also called intrahepatic cholestasis of pregnancy, is a pregnancy specific liver disorder that affects about 1 in 200 women in the UK. It typically presents in the third trimester with maternal pruritus and deranged liver function, including raised serum bile acids. The maternal symptoms and biochemical abnormalities resolve rapidly after delivery and severe OC is therefore considered to be a cause of transient hepatic impairment for the mother. However, severe OC is associated with an increased incidence of adverse fetal outcomes, including spontaneous preterm labour, fetal distress (both antenatally and during labour) and sudden intrauterine death[1].

The aetiologies of the maternal disease and the fetal complications associated with the condition are not completely understood. Despite this, there are several lines of evidence suggesting that the adverse outcomes may be due to the toxic effects of bile acids, and several studies have demonstrated a correlation between the maternal serum bile acid level and the risk of adverse fetal events[2][3][4][5]. The most definitive of these studies investigated the incidence of OC and of the adverse fetal outcomes in a Swedish population of 45,000 women, of whom 690 women were diagnosed with OC[2]. The data from this study demonstrate that the risk of meconium staining of the amniotic fluid, green staining of the placenta and fetal membranes, asphyxial events and preterm delivery is increased by 1-2% for every additional 1 mmol/L of maternal serum bile acids. However, this did not reach statistical significance for women with mild or moderate elevations in maternal fasting serum bile acid levels, but was significant for those with severe cholestasis defined as fasting serum bile acid levels greater than 40 mmol/L.

Several small studies have reported the incidences of adverse fetal outcomes in the UK population[6][7], but none have been able to demonstrate a correlation with maternal serum bile acid level.


  • To use the UK Obstetric Surveillance System to describe the incidence, management and outcome of pregnancies in women with severe obstetric cholestasis in the UK.

Research questions

  • What is the current incidence of severe obstetric cholestasis in the UK?
  • What management strategies are used for in women with severe obstetric cholestasis? In particular what is the incidence of elective preterm delivery and the use of ursodeoxycholic acid treatment?
  • What complications are seen during pregnancy in women with severe obstetric cholestasis?
  • What are the outcomes for mother and infant?

Case definition

Any woman in the UK identified as having severe obstetric cholestasis using the following definition:

  • Pruritus in the absence of a rash and in association with a single maternal serum bile acid level greater than 40 mmol/L at any time point in the pregnancy

Excluded: Women with obstetric cholestasis but with bile acid levels less than 40 mmol/L.


Wellbeing of Women

Ethics committee approval

The study has been approved by the London MREC (study ref 10/H0718/20).


Professor Catherine Williamson, Institute of Reproductive and Developmental Biology, Imperial College London

Dr Victoria Geenes, Institute of Reproductive and Developmental Biology, Imperial College London

Dr Marian Knight, National Perinatal Epidemiology Unit, University of Oxford

Download the Data Collection Form (DCF)

Cholestasis in Pregnancy Form


  1. ^ Geenes, V., et al., World J Gastroenterol 2009; 2049-2066.
  2. a, b Glantz, A., et al., Hepatology 2004; 40: 467-474.
  3. ^ Lee, R.H., et al., Am J Perinatol 2008; 25(6): 341-345.
  4. ^ Laatikainen, T., and Ikonen, E., Obst Gynecol 1977; 50(3): 313-318.
  5. ^ Laatikainen, T., and Tulenheimo., Int J Gynaecol Obstet 1984; 22(2): 91-94.
  6. ^ Williamson, C., et al., BJOG 2004; 111: 676-681.
  7. ^ Kenyon, A.P., et al., BJOG 2002; 109: 282-288.

Updated: Tuesday, 17 January 2023 18:16 (v5)