Carlos Carreno

Excessive Early Gestational Weight Gain And Risk of Gestational Diabetes Mellitus in Nulliparous Women

OBJECTIVE: To estimate whether there is an association between excessive early gestational weight gain and the development of gestational diabetes mellitus (GDM) and excessive fetal growth. METHODS: This is a secondary analysis of a randomized controlled trial of vitamins C and E in nulliparous low-risk women. Maternal weight gain from prepregnancy (self-reported) to 15–18 weeks of gestation was measured, and expected gestational weight gain was determined using the Institute of Medicine 2009 guidelines for each prepregnancy body mass index category. Excessive early gestational weight gain was defined as gestational weight gain greater than the upper range of the Institute of Medicine guidelines. Rates of GDM, birth weight greater than 4,000 g, and large for gestational age (LGA, birth weight 90th percentile or higher) were calculated and compared between women with excessive early gestational weight gain and early nonexcessive gestational weight gain (within or below Institute of Medicine guidelines). RESULTS: A total of 7,985 women were studied. Excessive early gestational weight gain occurred in 47.5% of women. Ninety-three percent of women with excessive early gestational weight gain had total gestational weight gain greater than Institute of Medicine guidelines. In contrast, only 55% of women with nonexcessive early gestational weight gain had total gestational weight gain greater than Institute of Medicine guidelines (P<.001). Rates of GDM, LGA, and birth weight greater than 4,000 g were higher in women with excessive early gestational weight gain. CONCLUSION: In our population, excessive early gestational weight gain occurred in 93% of women who had total gestational weight gain greater than the Institute of Medicine guidelines. In low-risk nulliparous women, excessive early gestational weight gain is associated with the development of GDM and excessive fetal growth. LEVEL OF EVIDENCE: II

Overestimation of fetal weight by ultrasound: does it influence the likelihood of cesarean delivery for labor arrest?

OBJECTIVEnWe sought to determine whether the overestimation of ultrasound-derived estimated fetal weight (EFW) is associated with increased diagnosis of labor arrest.nnnSTUDY DESIGNnThis is a historical cohort study of nulliparous women with term pregnancies who underwent bedside ultrasound examination for EFW before labor induction. Labor outcomes of women with EFW overestimation > 15% the actual birthweight were compared with those with EFW not overestimated.nnnRESULTSnOverestimation of EFW occurred in 9.5% of cases (23/241). The rate of cesarean delivery (CD) for labor arrest was higher for those with EFW overestimation (34.8% vs 13.3%; P = .01) even though there were no differences in length of the induction duration. After adjusting for confounding factors, EFW overestimation remained associated with CD for labor arrest (odds ratio, 4.8; 95% confidence interval, 1.5-15.2).nnnCONCLUSIONnOur finding suggests that an overestimation of EFW may be associated with a lower threshold for CD for labor arrest.

The frequency of prior antenatal corticosteroid therapy in late preterm birth pregnancies

We sought to quantify how often women with late preterm birth (LPTB) receive antenatal corticosteroid (ACS) therapy prior to 34 weeks and to determine its effects on neonatal respiratory morbidity. LPTBs (34 (0)/ (7) to 36 (6)/ (7) weeks) over a 1-year period at a single tertiary care hospital were studied. A composite neonatal respiratory outcome was defined as mechanical ventilation, continuous positive airway pressure with fraction of inspired oxygen (F IO(2)) >40% for >2 hours or F IO(2) >40% for >4 hours within the first 72 hours of life. Multivariate logistic regression analysis was used to evaluate the association between ACS therapy and neonatal respiratory morbidity. Over the study period, 503 LPTBs met the study criteria and 6.8% ( Nu2009=u200934) had ACS therapy <34 weeks. Most had exposure >7 days prior to delivery (64.7%). Almost one-half of those receiving prior ACS therapy delivered between 34 and 35 weeks. There was no difference in the rate of prior ACS therapy based on LPTB indication for delivery. After adjusting for confounding factors, prior ACS therapy was not associated with lower respiratory morbidity (odds ratio [OR] 2.0, 95% confidence interval [CI] 0.2 to 16.3, Pu2009=u20090.53). Advancing gestational age was the only variable associated with respiratory morbidity (OR 0.50, 95% CI 0.26 to .94, Pu2009=u20090.03). In our population, prior ACS therapy was infrequent and was not associated with improvements in neonatal respiratory morbidity following LPTB.

Corticosteroids effect on caspase 3 expression in an in-vitro model of hypoxic brain cells

Abstract Objective: Effects of corticosteroids (CS) in the brain of growth-restricted fetus remain largely unstudied. We investigated if dexamethasone (DXM) exposure contributes to neuronal injury in an in-vitro model of neuronal cells under hypoxic conditions (surrogate for fetal growth restriction). Study design: U87 glioblastoma cells exposed to hypoxic or normoxic conditions for 10u2009h were incubated in the absence or presence of DXM for 48u2009h. Apoptosis as possible indicator of neurotoxicity was determined using a caspase-3-specific activity assay and western blotting. Caspase-3 was calculated as percentage of mean caspase-3 cleavage. Each experiment was performed in triplicate (nu2009=u200948). Caspase 3 activity in cell culture media was also measured by ELISA. Results: Pro-caspase-3 (32u2009kDa) was expressed in culture, but activated 17 Kd caspase 3 was not expressed in cell lysate. There was no difference in ratio of caspase 3 activation when U87 cells were exposed to 10 v of hypoxia as compared to normoxia (0.46u2009±u20090.44 versus 0.37u2009±u20090.37). The pro-apoptotic effects of DXM were not increased by pre-exposure to hypoxia: (0.37u2009±u20090.37 versus 0.47u2009±u20090.40). Conclusion: The addition of DXM to hypoxic U87 cells had no additive or synergistic effects on the activation of caspase 3. Therefore, we speculate that the administration of CS in the setting of fetal growth restriction would not lead to increased apoptosis with potential neuronal injury.