Department of Epidemiology, University of Pittsburgh Graduate School of Public Health, Pittsburgh, PA, USA.
Am J Clin Nutr. 2013 Aug;98(2):383-8. doi: 10.3945/ajcn.112.055426. Epub 2013 Jun 26.
Maternal vitamin D deficiency has been linked to fetal growth restriction, but the underlying mechanisms are unclear.
We tested the hypothesis that poor maternal 25-hydroxyvitamin D [25(OH)D] is associated with increased risk of placental vascular pathology.
Maternal serum 25(OH)D was measured at ≤26 wk of gestation in a random subcohort of term, singleton infants in the Collaborative Perinatal Project (1959-1966; n = 2048). A dichotomous vascular construct was created from the presence of any of 12 pathologies identified on placental examinations, including evidence of placental abruption, infarction, hypoxia, decidual vasculopathy, or thrombosis of fetal vessels (n = 240 cases).
The relation between 25(OH)D and vascular pathology was modified by infant sex (P = 0.003). A maternal 25(OH)D concentration ≥80 compared with <50 nmol/L was associated with 49% lower risk of pathology in boys [adjusted OR (95% CI): 0.27, 0.95] after conditioning on study site. No associations were observed between maternal 25(OH)D and pathology in mothers with female offspring. Subsequent analyses showed that, in pregnancies with a female fetus, vascular pathology was associated with a reduced birth-weight z score when the mother's 25(OH)D concentration was <30 nmol/L (β: -0.73; 95% CI: -1.17, -0.30). No association was observed between pathology and birth weight in mothers of female offspring with 25(OH)D concentrations ≥30 nmol/L or in boys, regardless of maternal 25(OH)D status.
Our findings suggest complex relations between vitamin D, placental vascular pathology, and birth weight that differ by infant sex. Maternal vitamin D status may be beneficial for male and female offspring through different mechanisms.
母体维生素 D 缺乏与胎儿生长受限有关,但潜在机制尚不清楚。
我们检验了这样一个假设,即母体 25-羟维生素 D [25(OH)D] 水平较差与胎盘血管病变风险增加有关。
在 1959-1966 年的协作围产期项目(Collaborative Perinatal Project)中,对≤26 孕周的足月、单胎婴儿的随机亚队列(n=2048)测量了母体血清 25(OH)D。从胎盘检查中发现的 12 种病变中的任何一种存在情况构建了一个二分类血管结构,包括胎盘早剥、梗死、缺氧、蜕膜血管病变或胎儿血管血栓形成的证据(n=240 例)。
25(OH)D 与血管病变之间的关系受到婴儿性别(P=0.003)的影响。与母体 25(OH)D 浓度<50 nmol/L 相比,浓度≥80 nmol/L 与男婴的病变风险降低 49%相关[调整后的比值比(95%可信区间):0.27,0.95],条件为研究地点。在女婴的母亲中,母体 25(OH)D 与病理学之间没有观察到相关性。进一步的分析表明,在怀有女婴的孕妇中,如果母亲的 25(OH)D 浓度<30 nmol/L,血管病变与出生体重 z 分数降低相关(β:-0.73;95%CI:-1.17,-0.30)。在女婴母亲中,母体 25(OH)D 浓度≥30 nmol/L 或男婴中,均未观察到病理与出生体重之间存在相关性,而不论母体 25(OH)D 状态如何。
我们的研究结果表明,维生素 D、胎盘血管病变和出生体重之间的关系复杂,且因婴儿性别而异。母体维生素 D 状态可能通过不同的机制对男婴和女婴都有益。