Background Obesity in pregnancy is common, with more than 50% of pregnant women being overweight or obese. Obesity has been identified as an independent predictor of dysfunctional labor and is associated with increased risk of failed induction of labor resulting in cesarean section. Leptin, an adipokine, is secreted from adipose tissue under the control of the obesity gene. Concentrations of leptin increase with increasing percent body fat due to elevated leptin production from the adipose tissue of obese individuals. Interestingly, the placenta is also a major source of leptin production during pregnancy. Leptin has regulatory effects on neuronal tissue, vascular smooth muscle, and nonvascular smooth muscle systems. It has also been demonstrated that leptin has an inhibitory effect on myometrial contractility with both intensity and frequency of contractions decreased. These findings suggest that leptin may play an important role in dysfunctional labor and be associated with the outcome of induction of labor at term. Our aim is to determine whether maternal plasma leptin concentration is indicative of the outcome of induction of labor at term. We hypothesize that elevated maternal plasma leptin levels are associated with a failed term induction of labor resulting in a cesarean delivery. Methods In this case-control study, leptin was measured in 3rd trimester plasma samples. To analyze labor outcomes, 174 women were selected based on having undergone an induction of labor (IOL), (115 women with successful IOL and 59 women with a failed IOL). Plasma samples and clinical information were obtained from the UI Maternal Fetal Tissue Bank (IRB# 200910784). Maternal plasma leptin and total protein concentrations were measured using commercially available assays. Bivariate analyses and logistic regression models were constructed using regression identified clinically significant confounding variables. All variables were tested at significance level of 0.05. Results Women with failed IOL had higher maternal plasma leptin values (0.5 vs 0.3 pg, P = 0.01). These women were more likely to have obesity (mean BMI 32 vs 27 kg/m2, P = 0.0002) as well as require multiple induction methods (93% vs 73%, p = 0.008). Logistic regression showed Bishop score (OR 1.5, p < 0.001), BMI (OR 0.92, P < 0.001), preeclampsia (OR 0.12, P = 0.010), use of multiple methods of induction (OR 0.22, P = 0.008) and leptin (OR 0.42, P = 0.017) were significantly associated with IOL outcome. Specifically, after controlling for BMI, Bishop Score, and preeclampsia, leptin was still predictive of a failed IOL with an odds ratio of 0.47 (P = 0.046). Finally, using leptin as a predictor for fetal outcomes, leptin was also associated with of fetal intolerance of labor, with an odds ratio of 2.3 (P = 0.027). This association remained but failed to meet statistical significance when controlling for successful (IOL) (OR 1.5, P = 0.50). Conclusions Maternal plasma leptin may be a useful tool for determining which women are likely to have a failed induction of labor and for counseling women about undertaking an induction of labor versus proceeding with cesarean delivery.
During pregnancy, there are normal changes in maternal body weight and blood pressure that occur. Leptin is found in higher levels in obese individuals and has been demonstrated to have an inhibitory effect on myometrial contractility and to regulate blood pressure. Obesity in pregnancy is common and is associated with many complications, including hypertension in pregnancy, failed induction of labor (IOL), and intrauterine growth restriction. Our goal was to determine whether maternal leptin in a pregnant population is indicative of hypertensive disorders in pregnancy, dysfunctional labor, and whether there is a correlation between cord blood leptin and birthweight. We utilized a case control study with samples from the UI Maternal Fetal Tissue Bank (IRB#200910784). In order to analyze labor outcomes, 168 women were selected based on having undergone an IOL, including 54 failed IOL. Maternal/neonatal characteristics were collected from the medical record. Maternal and cord blood plasma leptin and total protein levels were measured using commercially available ELISAs. Bivariate analyses and logistic regression models were constructed using regression identified clinically-significant confounding variables. All variables were tested at significance level of 0.05. Women with hypertensive disorders in pregnancy, including pregnancy-induced hypertension and preeclampsia, had higher maternal leptin levels (14783 vs. 21440 pg/mL, p=0.049). Women with failed IOL also had higher maternal plasma leptin values (0.5 vs 0.3 leptin/protein [pg/ug], P = 0.01). Birthweight was also correlated with cord blood leptin (correlation coefficient 0.494 P < 0.001). These data suggest that maternal and fetal leptin levels are associated with the central mechanisms responsible for poor pregnancy outcomes.
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