438: The impact of change in pregnancy body mass index on preterm birth and low birthweight

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index on preterm birth and low birthweight Morgan Swank, Aaron Caughey, Christine Farinelli, Elliott Main, Kathryn Melsop, William Gilbert, Judith Chung University of California, Irvine, Maternal Fetal Medicine, Orange, CA, Oregon Health & Science University, Maternal Fetal Medicine, Portland, OR, California Maternal Quality Care Collaborative, CMQCC, Stanford, CA, Sutter Medical Center, Maternal Fetal Medicine, Sacramento, CA OBJECTIVE: To examine the impact of gestational change in body mass index (BMI) on preterm birth and low birthweight, accounting for pregnancy duration. STUDY DESIGN: Retrospective cohort study using linked birth certificate and discharge diagnosis data (All-California, Rapid-Cycle, Maternal/Infant Database) from the year 2007. To account for differences in gestational age at delivery, average weekly weight gain was calculated and then standardized to a 40 week gestation. Unadjusted and adjusted odds ratios with 95% confidence intervals were calculated for the outcomes of birth prior to 34 weeks’ gestation (PTB) and low birthweight (LBW), defined as 2500 grams, as a function of change in pregnancy BMI. Change in BMI, was treated as a categorical variable: BMI loss (BMI change -0.5), no change (-0.5 to 0.5), minimal (0.6 to 5), moderate (5.1 to 10), and excessive ( 10), with no change in BMI serving as the reference group. The impact of pregnancy change in BMI was determined for the entire cohort and then stratified by pre-pregnancy WHO BMI category. RESULTS: The study population consisted of 436,414 women. Women with BMI loss had the highest odds of PTB (aOR 1.30, 95% CI 1.07-1.57), when compared to those with no net change in BMI. Women with excessive BMI change also had an increased odds of PTB (aOR 1.21; 95% CI 1.04-1.40), while those with minimal (aOR 0.60, 95% CI 0.52-0.69) and moderate (aOR 0.52, 95% CI 0.45-0.60) change, had a reduced odds of PTB. LBW was only increased in women with BMI loss (aOR 1.41, 95% CI 1.23-1.62). When stratified by prepregnancy BMI, women with a starting BMI in obese classes I-III were the driving force behind the increased odds of PTB among those with excessive BMI change. CONCLUSION: While BMI loss in pregnancy may be undesirable, due to its association with an increased odds of PTB and LBW, excessive BMI change among obese women may also be disadvantageous, due to an increased odds of PTB seen in our study. 439 Placental mitochondrial stress and mitochondrial morphology in a baboon model of maternal obesity Natalia Schlabritz-Loutsevitch, Yao Sun, Robert Ahokas, Robert Ferry, Gene Hubbard, Giancarlo Mari University of Tennessee Health Science Center, Obstetrics and Gynecology, Memphis, TN, University of Tennesse Health Science Center, Department of Cardiology, Memphis, TN, University of Tennessee Health Science Center, Pediatrics, Memphis, TN, University of Texas Health Science Center at San Antonio, Pathology, San Antonio, TX OBJECTIVE: Placental mitochondrial stress has been described in maternal obesity, pre-eclampsia, and intrauterine growth restriction. Mitochondrial stress is associated with apoptosis and generation of reactive oxygen species (ROS) through NADPH oxidase (NOX) activity. NOX comprises a group of five enzymes, NOX 1-5. NOX 2 is expressed in the placental Hoffbauer cells and neutrophils. We and others previously described placental infiltration by macrophages and neutrophils in maternal obesity. Objectives of this study were to: 1) assess placental NOX-2 protein expression and activity as well as morphology of endothelial (E), cytotrophoblast (CT), and syncytiotrophoblast (ST) mitochondria; 2) measure placental apoptosis and proliferation in obese and non-obese placentas. STUDY DESIGN: Placentas from obese (n 4) and non-obese (n 4) baboons near term were retrieved and processed as previously described (Farley et al., 2009). Placental NOX-2 protein was quantified by Western blot of tissue lysates, localized by immunohistochemistry, and assessed functionally by activity assay. Placental mitochondria were measured on electron micrographs using isometric point intersect method. Placenta was stained with KI-67 to access proliferation and TUNNEL staining was used to evaluate placental apoptosis. RESULTS: NOX-2 protein level directly correlated with placental apoptosis (r 0.80, p 0.05) and with mitochondrial volume in E (but not in CT and ST) (r 0.81, p 0.05). There were no differences in placental NOX-2 activity and protein expression, mitochondrial volume, or placental proliferation/apoptosis between obese and non-obese animals. CONCLUSION: Placental NOX-2 localizes not only to Hoffbauer cells and neutrophils, but is also shown for the first time within the fetal endothelium of this non-human primate model. Such localization of NOX-2 has been described in human endothelia damaged by atherosclerosis or myocardial infarction. Release of ROS by macrophages/ neutrophils may directly influence the fetal vascular system.