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down Lisa M. Bodnar, Janet M. Catov, Hyagriv N. Simhan, Michael F. Holick, Robert W. Powers, and James M. Roberts
Maternal Vitamin D Deficiency Increases the Risk of Preeclampsia
J. Clin. Endocrinol. Metab. 92: 3517-3522; published online before print as doi:10.1210/jc.2007-0718


Abstract 1 of 1 back The Journal of Clinical Endocrinology & Metabolism Vol. 92, No. 9 3517-3522
Copyright © 2007 by The Endocrine Society

Maternal Vitamin D Deficiency Increases the Risk of Preeclampsia

Lisa M. Bodnar, Janet M. Catov, Hyagriv N. Simhan, Michael F. Holick, Robert W. Powers and James M. Roberts

Department of Epidemiology (L.M.B., J.M.C., J.M.R.), University of Pittsburgh Graduate School of Public Health, Pittsburgh, Pennsylvania 15261; Department of Obstetrics, Gynecology, and Reproductive Sciences (L.M.B., J.M.C., H.N.S., R.W.P., J.M.R.), University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261; Magee-Womens Research Institute (L.M.B., J.M.C., H.N.S., R.W.P., J.M.R.), Pittsburgh, Pennsylvania 15213; and Vitamin D Laboratory (M.F.H.), Section of Endocrinology, Nutrition and Diabetes, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02115

Address all correspondence and requests for reprints to: Lisa M. Bodnar, Ph.D., M.P.H., R.D., Department of Epidemiology, University of Pittsburgh Graduate School of Public Health, A742 Crabtree Hall, 130 DeSoto Street, Pittsburgh, Pennsylvania, 15261. E-mail: bodnar{at}edc.pitt.edu.

Context: Vitamin D has direct influence on molecular pathways proposed to be important in the pathogenesis of preeclampsia, yet the vitamin D-preeclampsia relation has not been studied.

Objectives: We aimed to assess the effect of maternal 25-hydroxyvitamin D [25(OH)D] concentration on the risk of preeclampsia and to assess the vitamin D status of newborns of preeclamptic mothers.

Design and Setting: We conducted a nested case-control study of pregnant women followed from less than 16 wk gestation to delivery (1997–2001) at prenatal clinics and private practices.

Patients: Patients included nulliparous pregnant women with singleton pregnancies who developed preeclampsia (n = 55) or did not develop preeclampsia (n = 219). Women’s banked sera were newly measured for 25(OH)D.

Main Outcome Measure: The main outcome measure was preeclampsia (new-onset gestational hypertension and proteinuria for the first time after 20 wk gestation). Our hypotheses were formulated before data collection.

Results: Adjusted serum 25(OH)D concentrations in early pregnancy were lower in women who subsequently developed preeclampsia compared with controls [geometric mean, 45.4 nmol/liter, and 95% confidence interval (CI), 38.6–53.4 nmol/liter, vs. 53.1 and 47.1–59.9 nmol/liter; P < 0.01]. There was a monotonic dose-response relation between serum 25(OH)D concentrations at less than 22 wk and risk of preeclampsia. After confounder adjustment, a 50-nmol/liter decline in 25(OH)D concentration doubled the risk of preeclampsia (adjusted odds ratio, 2.4; 95% CI, 1.1–5.4). Newborns of preeclamptic mothers were twice as likely as control newborns to have 25(OH)D less than 37.5 nmol/liter (adjusted odds ratio, 2.2; 95% CI, 1.2–4.1).

Conclusions: Maternal vitamin D deficiency may be an independent risk factor for preeclampsia. Vitamin D supplementation in early pregnancy should be explored for preventing preeclampsia and promoting neonatal well-being.

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