Preeclampsia contributes to neonatal morbidity and mortality due to prematurity and intrauterine growth restriction (IUGR) from uteroplacental vascular insufficiency. Studies of infant growth or developmental outcome after preeclampsia suffer from lack of regor in definitions of IUGR and preeclampsia, as well as a reliance on the insensitive measure of birth weight to identify affected infants. Preeclampsia is also associated with maternal metabolic derangements, including altered prostaglandin and lipid metabolism, increased vascular reactivity, and increased lipid peroxidation. Data suggest that maternal systemic disease is due to circulating factors which alter endothelial function. In Dr. Roberts' laboratory, similar factors were found with umbilical cord blood from preeclamptic pregnancies. The relationship of these biochemical and cellular aberrations to fetal well-being has not been investigated.
The AIM of this project is to obtain pilot data for a prospective longitudinal study to examine, using quantitative noninvasive tools, the growth and neurodevelopmental outcome of infants of preeclamptic women. Study groups consist of infants from pregnancies diagnosed with maternal preeclampsia (Group I), transient hypertension without proteinuria (Group 2), or normotensive uncomplicated pregnancies (Group 3). All infants will be fullterm and of appropriate brithweight for gestational age (AGA). Fetal pathophysiology will be assessed by lipid analyses of umbilical cord blood and a pathologist's examination of the placenta. Infant size, body composition and neuromaturation will be evaluated at birth, 4 months, and 12 months of age. Body composition will be assessed by total body electrical conductance. Neuromaturation will be assessed by electroencephalographic sleep recordings, visual evoked response studies, and neurodevelopmental examinations. We hypothesize that infants who experienced preeclampsia will show impaired growth, adiposity and neurophysiological maturation. We further predict a negative relationship between altered fetal lipid profiles and neonatal outcome. This project will provide the most thorough examination of neunatal status after preeclampsia to date. It will also be the first to investigate relationships betwen putative mechanisms of maternal and fetal pathophysiology in preeclampsia and infant outcome.
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Hux, Vanessa J; Roberts, James M; Okun, Michele L (2017) Allostatic load in early pregnancy is associated with poor sleep quality. Sleep Med 33:85-90 |
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Gandley, Robin E; Althouse, Andrew; Jeyabalan, Arundhathi et al. (2016) Low Soluble Syndecan-1 Precedes Preeclampsia. PLoS One 11:e0157608 |
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Luiza, John W; Gallaher, Marcia J; Powers, Robert W (2015) Urinary cortisol and depression in early pregnancy: role of adiposity and race. BMC Pregnancy Childbirth 15:30 |
Hux, Vanessa J; Roberts, James M (2015) A potential role for allostatic load in preeclampsia. Matern Child Health J 19:591-7 |
Hassis, Maria E; Niles, Richard K; Braten, Miles N et al. (2015) Evaluating the effects of preanalytical variables on the stability of the human plasma proteome. Anal Biochem 478:14-22 |
Catov, Janet M; Abatemarco, Diane; Althouse, Andrew et al. (2015) Patterns of gestational weight gain related to fetal growth among women with overweight and obesity. Obesity (Silver Spring) 23:1071-8 |
Founds, Sandra A; Ren, Dianxu; Roberts, James M et al. (2015) Follistatin-like 3 across gestation in preeclampsia and uncomplicated pregnancies among lean and obese women. Reprod Sci 22:402-9 |
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