W6.2 High prepregnancy body mass index is associated with low PlGF in preeclampsia and uncomplicated pregnancies

Abstract

W6.4 – Table 1 Group 4 to 15 weeks gestation 15.1 to 25 weeks gestation 25.1 to 33 weeks gestation 33.1 to 42 weeks gestation Lean/Control 0.32 [0.27-0.39] 0.30 [0.24-0.36] 0.31 [0.25-0.36] 0.34 [0.28-0.39] Overweight-Obese/Control 0.39 [0.34-0.47]* 0.42 [0.37-0.48]* 0.40 [0.35-0.46]* 0.43 [0.35-0.49]* Lean/Preeclampsia 0.44 [0.37-0.51]* 0.39 [0.30-0.48]* 0.44 [0.36-0.49]* 0.48 [0.37-0.55]* Overweight-Obese/Preeclampsia 0.44 [0.36-0.54]*# 0.47 [0.41-0.51]* 0.54 [0.46-0.58]*# 0.51 [0.43-0.56]*# Data are median [interquartile range], *p 25 kg/m2. Obesity may influence the risk of preeclampsia by negatively affecting maternal PlGF concentrations. Supported by National Institutes of Health grant number P01-HD30367 and Abbott Laboratories. W6.3 Central adiposity influences the lipid response to pregnancy and is associated with reduced vascular function Eleanor Jarvie, Frances Stewart, Muriel Caslake, Jane Ramsay, William Ferrell, Dilys Freeman. University of Glasgow, Glasgow, UK Central adiposity is a risk factor for pre-eclampsia. Maternal obesity is associated with an inappropriate metabolic adaptation to pregnancy which may provoke the maternal endothelial dysfunction characteristic of preeclampsia. Adipose tissue depots have different metabolic activities and location of fat storage either at the outset of pregnancy or accumulated during pregnancy may be critical to the gestational metabolic response. We examined whether body fat distribution at booking determines the metabolic response to pregnancy and vascular function. In 60 women at booking, upper body subcutaneous (USAT) and visceral adipose tissue (UVAT) thicknesses were assessed by ultrasound. Lower body subcutaneous fat (LSAT) was assessed by hip circumference. Endothelium-dependent microvascular function (EDMVF) determined by laser Doppler iontophoresis and plasma markers of lipid & carbohydrate metabolism and inflammation were assessed in the 1st, 2nd and 3rd trimester. Baseline USAT is positively associated with baseline inflammatory status and contributes to 8.4% (p=0.009) and 11.2% (p=0.004) of the variation in baseline IL-6 and CRP respectively, independent of other adipose tissue depots. Baseline UVAT is negatively associated with baseline EDMVF (7.7%, p=0.025). UVAT is associated with an increased sVCAM-1 exposure [total area under the curve (AUC) 30.0%, p=0.003] and USAT is associated with a reduction in EDMVF (9.9%, p=0.027) throughout pregnancy. Lipid mobilisation, assessed as incremental AUC of VLDL-1 (p=0.005) and VLDL-2 (p=0.004) concentrations, was lower in women with large UVAT but higher in those with large USAT (p=0.014). UVAT is associated with endothelial activation and a less flexible lipid response to pregnancy. USAT is related to chronic inflammation at the outset and with poor microvascular function over the course of pregnancy. Upper body adiposity influences the metabolic and vascular adaptation to pregnancy and may be the mechanism by which maternal central adiposity increases risk of preeclampsia. W6.4 Plasma ADMA is elevated throughout pregnancy in women who develop preeclampsia and is accentuated by pre-pregnancy obesity Robert Powers, James Roberts, Arun Jeyabalan, Robin Gandley, Carl Hubel. University of Pittsburgh, USA Context: Vascular dysfunction is an important aspect of the pathophysiology of preeclampsia. Pre-pregnancy obesity is an independent risk factor for preeclampsia. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase. ADMA is an emerging risk factor for vascular disease and is elevated in obesity. Objective: The aim of the study was to investigate the concentration of maternal ADMA across pregnancy, and the association of ADMA to obesity and pregnancy outcome. Study design: Maternal plasma ADMA was quantified by HPLC in longitudinal samples from 50 women who developed preeclampsia and 100 controls who remained normotensive. Data were analyzed by ANOVA and significance accepted at p<0.05. Results: Maternal plasma ADMA was significantly elevated throughout pregnancy in subjects who developed preeclampsia compared to controls (p<0.01). ADMA was significantly elevated in overweight-obese controls compared to lean controls throughout pregnancy (p<0.05, table). ADMA was significantly elevated throughout pregnancy among lean subjects who developed preeclampsia compared to lean controls (p<0.05, table). ADMA was also significantly elevated among overweight-obese subjects who