Abstract

BackgroundIt is crucial to identify in large population samples the most important determinants of excessive fetal growth. The aim of the study was to evaluate the independent role of pre-pregnancy body mass index (BMI), gestational weight gain and gestational diabetes on the risk of macrosomia.MethodsA prospective study collected data on mode of delivery and maternal/neonatal outcomes in eleven Hospitals in Italy. Multiple pregnancies and preterm deliveries were excluded. The sample included 14109 women with complete records. Associations between exposure variables and newborn macrosomia were analyzed using Pearson’s chi squared test. Multiple logistic regression models were built to assess the independent association between potential predictors and macrosomia.ResultsMaternal obesity (adjusted OR 1.7, 95% CI 1.4-2.2), excessive gestational weight gain (adjusted OR 1.9, 95% CI 1.6-2.2) and diabetes (adjusted OR 2.1, 95% CI 1.5-3.0 for gestational; adjusted OR 3.0, 95% CI 1.2-7.6 for pre-gestational) resulted to be independent predictors of macrosomia, when adjusted for other recognized risk factors. Since no significant interaction was found between pre-gestational BMI and gestational weight gain, excessive weight gain should be considered an independent risk factor for macrosomia. In the sub-group of women affected by gestational or pre-gestational diabetes, pre-gestational BMI was not significantly associated to macrosomia, while excessive pregnancy weight gain, maternal height and gestational age at delivery were significantly associated. In this sub-population, pregnancy weight gain less than recommended was not significantly associated to a reduction in macrosomia.ConclusionsOur findings indicate that maternal obesity, gestational weight gain excess and diabetes should be considered as independent risk factors for newborn macrosomia. To adequately evaluate the clinical evolution of pregnancy all three variables need to be carefully assessed and monitored.

Highlights

  • It is crucial to identify in large population samples the most important determinants of excessive fetal growth

  • It is already well known that both obesity and Gestational diabetes (GDM) are relative risk factors for adverse maternal and neonatal outcomes, being related to an increased occurrence of Large for Gestational Age (LGA) fetuses and macrosomia

  • Our findings suggest that maternal obesity, excessive gestational weight gain and diabetes are independent valuable predictors of macrosomia, when adjusted for other recognized risk factors

Read more

Summary

Introduction

It is crucial to identify in large population samples the most important determinants of excessive fetal growth. The aim of the study was to evaluate the independent role of pre-pregnancy body mass index (BMI), gestational weight gain and gestational diabetes on the risk of macrosomia. The incidence of obesity and gestational diabetes (GDM) is rising worldwide. The prevalence of obesity, defined as a Body Mass Index (BMI) equal or over 30 Kg/m2, increased from 12% in 1991 to 17.9% in 1998, in the U.S.A. It is already well known that both obesity and GDM are relative risk factors for adverse maternal and neonatal outcomes, being related to an increased occurrence of Large for Gestational Age (LGA) fetuses and macrosomia (defined as neonates birthweight over 4000 g). Maternal overweight and the related metabolic changes such as diabetes mellitus type 2 and GDM, seem to be crucially important

Objectives
Methods
Results
Discussion
Conclusion

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.