Bodnar Lisa M, Catov Janet M, Simhan Hyagriv N, Holick Michael F, Powers Robert W, Roberts James M
Department of Epidemiology, University of Pittsburgh Graduate School of Public Health, A742 Crabtree Hall, 130 DeSoto Street, Pittsburgh, Pennsylvania, 15261, USA.
J Clin Endocrinol Metab. 2007 Sep;92(9):3517-22. doi: 10.1210/jc.2007-0718. Epub 2007 May 29.
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.
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.
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 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.
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.
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).
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.
维生素D对先兆子痫发病机制中被认为重要的分子途径有直接影响,但维生素D与先兆子痫的关系尚未得到研究。
我们旨在评估孕妇25-羟维生素D[25(OH)D]浓度对先兆子痫风险的影响,并评估先兆子痫母亲所生新生儿的维生素D状态。
我们在产前诊所和私人诊所对妊娠小于16周直至分娩(1997 - 2001年)的孕妇进行了一项巢式病例对照研究。
患者包括单胎妊娠的初产妇,其中发生先兆子痫的有55例,未发生先兆子痫的有219例。新检测了这些女性储存的血清中的25(OH)D。
主要结局指标为先兆子痫(妊娠20周后首次出现新发妊娠期高血压和蛋白尿)。我们的假设在数据收集之前就已制定。
与对照组相比,随后发生先兆子痫的女性在妊娠早期经校正的血清25(OH)D浓度更低[几何平均数,45.4 nmol/L,95%置信区间(CI),38.6 - 53.4 nmol/L,对照组为53.1及47.1 - 59.9 nmol/L;P < 0.01]。妊娠小于22周时血清25(OH)D浓度与先兆子痫风险之间存在单调剂量反应关系。在对混杂因素进行校正后,25(OH)D浓度下降50 nmol/L使先兆子痫风险增加一倍(校正比值比,2.4;95% CI,1.1 - 5.4)。先兆子痫母亲所生新生儿的25(OH)D低于37.5 nmol/L的可能性是对照组新生儿的两倍(校正比值比,2.2;95% CI,1.2 - 4.1)。
母体维生素D缺乏可能是先兆子痫的一个独立危险因素。应探索在妊娠早期补充维生素D以预防先兆子痫并促进新生儿健康。