(721) Umbilical artery endocan level increases with maternal BMI

Maternal obesity is strongly associated with offspring obesity and is potentially inherited through fetal programming, for which inflammation and endothelial dysfunction may play a mediating role. Endocan is a soluble biomarker linked to endothelial dysfunction and inflammation. We sought to determine whether umbilical artery endocan levels at birth differed between newborns born to mothers with and without obesity.

Study Design:

We conducted a prospective cohort study of term mother/fetus dyads who presented for delivery. We collected umbilical artery cord blood at delivery, and measured fetal/cord endocan levels by ELISA. We assessed differences using statistical regression modeling. A sample size of 168 was planned to detect a difference of 35% between infants born to obese and non-obese mothers.

Results:

We recruited 233 patients; following exclusion criteria and dropout, 148 remained. BMI of the included mothers ranged from 21 to 97 kg/m² (median 34, IQR 8). There were 36 patients with BMI < 30 and 112 patients with BMI ≧ 30. Bivariate analysis using obesity as a dichotomous variable showed no difference in cord endocan level between patients with BMI < 30 and those with BMI ≧ 30 (medians 272 pg/ml [IQR 113] vs. 299 [153], p=0.476). A backward stepwise linear regression included the following candidate variables which were selected a priori: BMI at delivery, age, diabetes, hypertension, delivery mode, birthweight, sex. The final model reduced to BMI at delivery and maternal age. The overall regression was statistically significant (R²=0.12, F(2,142)=9.22, p< 0.001). Endocan levels in newborn cord blood were positively and significantly associated with maternal BMI at delivery (p = 0.022), when controlling for maternal age.

Conclusion:

Our results suggest that infants born to mothers with obesity may have higher levels of endothelial dysfunction and inflammation at birth, and may be affected in a dose-dependent manner with increasing BMI. These findings emphasize the importance of fetal programming in utero, prior to postnatal factors that contribute to downstream effects of maternal obesity.