Determinants of hepatic steatosis and increased liver stiffness in late pregnancy: analysis of 3000 women using transient elastography

Manna Luiza Borges; Christos Chatzakis; Caroline Ovadia; Catherine Williamson; Michael Heneghan; Kypros Nicolaides

doi:10.1530/endoabs.109.P163

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Endocrine Abstracts (2025) 109 P163 | DOI: 10.1530/endoabs.109.P163

SFEBES2025 Poster Presentations Metabolism, Obesity and Diabetes (68 abstracts)

Determinants of hepatic steatosis and increased liver stiffness in late pregnancy: analysis of 3000 women using transient elastography

Luiza Borges Manna ¹ , Christos Chatzakis ¹ , Caroline Ovadia ² , Catherine Williamson ³ , Michael Heneghan ⁴ & Kypros Nicolaides ¹

Author affiliations

¹Harris Birthright Research Centre for Fetal Medicine, Fetal Medicine Research Institute, King’s College Hospital, London, United Kingdom; ²Department of Women and Children’s Health, King’s College London, London, United Kingdom; ³Department of Metabolism, Digestion and Reproduction, Imperial College London, London, United Kingdom; ⁴Institute of Liver Studies, King’s College Hospital, London, United Kingdom

Background: Steatotic liver disease (SLD), a metabolic and hepatic disorder, is increasingly prevalent among reproductive-age women. Pregnancy can unmask maternal predispositions to future diseases, providing an opportunity to influence lifelong health. Understanding the relationship between SLD and pregnancy may enable early identification of at-risk women. This study aimed to investigate maternal and gestational factors associated with hepatic steatosis and increased liver stiffness in the third trimester.

Methods: 3000 pregnant women were recruited between 35+0- and 36+6-weeks’ gestation at the Harris Birthright Research Centre (London, United Kingdom). Exclusion criteria were chronic liver disease, alcohol intake >14 units/week pre-pregnancy and multifetal gestation. A FibroScan® was used to quantify Controlled Attenuation Parameter (CAP) and Liver Stiffness Measurement (LSM). The 90th percentiles of CAP (246dB/m) and LSM (7.1kPa) were used to define hepatic steatosis and increased liver stiffness, given the absence of gestation-specific reference ranges.

Results: 70.2% of participants were White, 15.9% Black, 7.4% South Asian, 1.9% East Asian, and 4.5% of mixed ethnicity. Median age and BMI were 34 years (interquartile range [IQR] 31-37) and 24.4 kg/m² (IQR 21.9-28.3), respectively. Factors associated with steatosis were obesity (odds ratio [OR] 11.7, 95%CI 8.01-17.2), overweight (OR 2.71, 95%CI 1.85-3.99) and maternal weight gain (OR 1.03, 95%CI 1.01-1.06). Increased LSM was associated with type 1 diabetes mellitus (OR 19.5, 95%CI 4.06-104), obesity (OR 1.94, 95%CI 1.3-2.87), previous fetal growth restriction (OR 2.43, 95%CI 1.19 – 4.62), previous gestational diabetes (OR 1.98, 95%CI 1.10-3.74), pre-eclampsia (OR 1.8, 95%CI 1.04-2.97), and nulliparity (OR 1.56, 95%CI 1.11-2.20).

Conclusion: Overweight and obese women, those with pre-eclampsia and a previous history of fetal growth restriction or gestational diabetes may benefit from enhanced postnatal surveillance to monitor their hepatic health. Future longitudinal studies should focus on these subgroups to better understand the natural course SLD in pregnancy and the postpartum period.