Relative impact of pre-eclampsia on birth weight in a low resource setting: A prospective cohort study.

Abstract

OBJECTIVES: Low birth-weight is a major risk factor for perinatal death in sub-Saharan Africa, but the relative contribution of determinants of birth-weight are difficult to disentangle in low resource settings. We sought to delineate the relationship between birth-weight and maternal pre-eclampsia across gestation in a low-resource obstetric setting. STUDY DESIGN: Prospective cohort study in a tertiary referral centre in urban Uganda, including 971 pre-eclampsia cases and 1461 control pregnancies between 28 and 42 weeks gestation. MAIN OUTCOME MEASURES: Nonlinear modeling of birth-weight versus maternal pre-eclampsia status across gestation. Models were adjusted for maternal-fetal characteristics including maternal age, parity, HIV status, and socio-economic status. Propensity score matching was used to control for the severity of pre-eclampsia at different gestational ages. RESULTS: Mean birth-weight for pre-eclampsia cases was 2.48 kg (±0.81SD) compared to 3.06 kg (±0.46SD) for controls (p < 0.001). At 28 weeks, the mean birth-weight difference between pre-eclampsia cases and controls was 0.58 kg (p < 0.05), narrowing to 0.17 kg at 39 weeks (p < 0.01). Controlling for pre-eclampsia severity only partially explained this gestational difference in mean birth-weight between pre-eclampsia cases and controls. Holding gestational age constant, pre-eclampsia status predicted 7.1-10.5% of total variation in birth-weight, compared to 0.05-0.7% for all other maternal-fetal characteristics combined. CONCLUSIONS: Pre-eclampsia is the dominant predictor of birth-weight in low-resource settings and hence likely to heavily influence perinatal survival. The impact of pre-eclampsia on birth-weight is smaller with advancing gestational age, a difference that is not fully explained by controlling for pre-eclampsia severity.CA is supported by an Isaac Newton Trust[12.21(a)]/Wellcome Trust ISSF [105602/Z/14/Z]/ University of Cambridge Joint Research Grant. This work was funded by the Wellcome Trust (094073/Z/10/B), and a Wellcome Trust Uganda Postdoctoral Fellowship in Infection and Immunity held by AN, funded by a Wellcome Trust Strategic Award, grant number 084344. Supported by NURTURE fellowship to AN, grant number D43TW010132. This work was also supported through the DELTAS Africa Initiative (grant number 107743/Z/15/Z). The DELTAS Africa Initiative is an independent funding scheme of the African Academy of Sciences (AAS)’s Alliance for Accelerating Excellence in Science in Africa (AESA) and supported by the New Partnership for Africa’s Development Planning and Coordinating Agency (NEPAD Agency) with funding from the Wellcome Trust (grant number 107743/Z/15/Z) and the UK government. The views expressed in this publication are those of the author(s) and not necessarily those of AAS, NEPAD Agency, Wellcome Trust or the UK government. JES acknowledges the support of a T32 fellowship from the U.S. National Institutes of Health

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