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Updated: Mar 25, 2026

Assessment of Maternal Vascular Remodeling During Pregnancy in the Mouse Uterus
Published on: December 5, 2015
An observational study of haemostatic changes, leptin and soluble endoglin during pregnancy in women with different
Ellie S Morgan1, Ellie Wilson, Therese Melody
1aDepartment of Anaesthesia, Royal Gwent Hospital, Newport bAcademic department of Anaesthesia, Critical Care and Resuscitation, Heart of England NHS Foundation Trust, Birmingham cDepartment of Thrombosis & Haemostasis, King's College and Thrombosis & Haemophilia Centre, Guy's & St Thomas' NHS Trust, London, United Kingdom dShanghai Institute of Planned Parenthood Research, Shanghai, China ePerioperative, Critical Care and Trauma Trials Group, School of Clinical and Experimental Medicine, University of Birmingham, United Kingdom.
Abstract:
Obesity increases the risk of venous thromboembolism (VTE) in pregnancy. The pathogenesis is hypothesized to be because of multiple factors including prothrombotic changes, but there has been minimal haemostatic research looking at the combined state of obesity and pregnancy. We aimed to determine whether variation in BMI in the third trimester of pregnancy was associated with prothrombotic changes. We recruited 110 women into four groups depending on their BMI at first antenatal appointment: normal, overweight, obese and morbidly obese. Women with increased risk of VTE, and/or receiving thromboprophylaxis, and/or more than 35 years and those in labour were excluded. Thromboelastography, platelet count, prothrombin time, activated partial thromboplastin time, fibrinogen, prothrombin fragment 1 + 2, free and total protein S, plasminogen activator inhibitor type 1, tissue plasminogen activator antigen, D-dimers, soluble endoglin and leptin levels were measured. There were no significant differences in haemostatic measures with changing BMI. There was a positive correlation between BMI and both platelet count (correlation coefficient r = 0.214, P = 0.036) and leptin (r = 0.435, P < 0.001), but only leptin had a significant association with BMI once adjusted for age, gestation and parity. Despite recruitment into the morbidly obese group being suboptimal, these findings suggest that in pregnancy, the increased risk of VTE seen in obese mothers is not mediated through increased prothrombotic changes, and thus the increased risk of VTE in obese pregnant women may be because of other mechanisms, for example endothelial dysfunction, inflammation and venous stasis.
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