Identifies risk factors for small-for-gestational-age infants in overweight/obese mothers, suggesting targeted interventions.
Introduction and Objective: Maternal obesity is strongly associated with fetal overgrowth, however, the association between maternal obesity and small-for-gestational-age (SGA) infants is less understood. This study aims to identify the factors associated with SGA in pregnancies affected by maternal overweight and obesity. Methods: This secondary analysis of the Vitamin D and Lifestyle Intervention for Gestational Diabetes Mellitus prevention (DALI) trial evaluated mothers with a body mass index (BMI) ≥29 kg/m2. Infants were classified as SGA (birthweight <10th percentile) and non-SGA, and maternal characteristics were compared between groups. Forward stepwise logistic regression was used to identify the predictors of SGA. Subgroup analysis stratified participants based on the presence of hypertensive disorders of pregnancy (HDP). Results: Of 748 included women (mean age 32.1±5.2 years, pre-pregnancy BMI 33.9±4.5kg/m2), 7.2% (n=54) had SGA. The SGA group had higher rates of unexplained prior stillbirth (30% vs. 10.4%, p=0.004), current hypertensive disorders (pregnancy induced hypertension: 23.1% vs. 10.9% p=0.01; preeclampsia 9.6% vs. 2.8%, p=0.02), and preterm birth (11.2 % vs. 3.9%, p<0.001) but lower cord blood glucose and cord serum leptin. In the regression analysis, preterm birth, primiparity, and maternal smoking were significantly associated with SGA (odds ratio with 95% CI: 12.14 (1.72-85.58), 6.73 (1.84-24.63), and 6.72 (1.86-24.28), respectively). For those with HDP, preterm birth was the only significant associated factor; for those without HDP, primiparity and maternal smoking remained the main predictors, along with a history of chronic hypertension. Low-density lipoprotein, triglycerides-glucose index, and maternal higher education were associated with a lower risk. Conclusion: Both modifiable and nonmodifiable risk factors exist for SGA in overweight/obese pregnancies. Further research is needed to guide targeted prevention and management strategies. Disclosure J. Immanuel: None. B.E. Reynolds: None. M. van Poppel: None. R. Corcoy Pla: None. L.T. Andersen: None. G. Desoye: None. A. Kautzky-Willer: None. P. Damm: None. J. Harreiter: None. D.J. Hill: None. D. Simmons: Speaker's Bureau; Ended; Novo Nordisk. Other - Educational grant; Ended; Abbott Diabetes. Research Support; Current; Novo Nordisk. Consultant; Ended; Dexcom, Inc. Funding This project received funding from the European Community’s 7th Framework Program (FP7/2007-2013; grant agreement no. 242187). In the Netherlands, additional funding was provided by the Netherlands Organization for Health Research and Development (ZonMW) (Grant nr 200310013). In the UK, the DALI team acknowledges the support received from the NIHR Clinical Research Network: Eastern, especially the local diabetes clinical and research teams based in Cambridge. In Spain, additional funding was provided by CAIBER 1527-B-226.
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