Reduced folate carrier 80A→G polymorphism, plasma folate, and risk of placental abruption
Reduced folate carrier 80A→G polymorphism, plasma folate, and risk of placental abruption
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DOI：
10.1007/s00439-008-0531-7
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发表时间：
2008-09-01
期刊：
影响因子：
5.3
通讯作者：
Rozen, Rima R.
中科院分区：
文献类型：
--
作者：
Ananth, Cande V.;Peltier, Morgan R.;Rozen, Rima R.
叶酸缺乏和母亲吸烟是胎盘早剥的重要危险因素。我们评估了还原叶酸载体[NM_194255.1：c.80A -> G（即，p.His27Arg）]（RFC-1）多态性与胎盘早剥相关，并评估母亲吸烟是否改变了血浆叶酸与胎盘早剥之间的关联。数据来源于新泽西州胎盘早剥研究--一项关于胎盘早剥的多中心病例对照研究（2002-2007）。使用PCR依赖性诊断测试分析母体DNA的RFC-1 c.80A -> G多态性。从分娩后立即收集的母体血浆中评估母体叶酸（nmol/l）。由于测定限制，叶酸水平>= 60 nmol/l时截短为60 nmol/l。因此，在调整潜在混杂因素后，通过删失对数正态回归模型评估叶酸的病例对照差异。RFC-1 c.80A -> G多态性的突变等位基因（G）在病例组（52.3%; n = 196）和对照组（50.5%; n = 191）之间的分布相似，纯合突变（G/G）基因型也相似（OR 1.1，95%CI 0.6-2.2）。在136例病例和140例对照的子样本中，胎盘早剥病例之间的分析检测限校正（平均值+/-标准误差）相似（63.6 +/- 5.1 nmol/l）和对照组（58.3 +/- 4.7 nmol/l; P = 0.270），母亲吸烟并没有改变这种关系（相互作用P = 0.169）。我们没有检测到RFC-1 c.80A -> G多态性与胎盘早剥之间的任何关联，血浆叶酸与胎盘早剥风险之间的关联也不明显。这些发现可能是产前多种维生素和叶酸补充剂在这一人群中的高流行率（超过80%）的结果。因此，叶酸缺乏可能是罕见的，并且RFC-1 c.80A -> G多态性对胎盘抑制的生物学意义较小，这并不奇怪。
Folate deficiency and maternal smoking are strong risk factors for placental abruption. We assessed whether the reduced folate carrier [NM_194255.1: c.80A -> G (i.e., p.His27Arg)] (RFC-1) polymorphism was associated with placental abruption, and evaluated if maternal smoking modified the association between plasma folate and abruption. Data were derived from the New Jersey-Placental Abruption Study-a multicenter, case-control study of placental abruption (2002-2007). Maternal DNA was assayed for the RFC-1 c.80A -> G polymorphism using a PCR-dependent diagnostic test. Maternal folate (nmol/l) was assessed from maternal plasma, collected immediately following delivery. Due to assay limitations, folate levels at >= 60 nmol/l were truncated at 60 nmol/l. Therefore, case-control differences in folate were assessed from censored log-normal regression models following adjustment for potential confounders. Distribution of the mutant allele (G) of the RFC-1 c.80A -> G polymorphism was similar between cases (52.3%; n = 196) and controls (50.5%; n = 191), as was the homozygous mutant (G/G) genotype (OR 1.1, 95% CI 0.6-2.2). In a sub-sample of 136 cases and 140 controls, maternal plasma folate levels (mean +/- standard error) corrected for assay detection limits were similar between placental abruption cases (63.6 +/- 5.1 nmol/l) and controls (58.3 +/- 4.7 nmol/l; P = 0.270), and maternal smoking did not modify this relationship (interaction P = 0.169). We did not detect any association between the RFC-1 c.80A -> G polymorphism and placental abruption, nor was an association between plasma folate and abruption risk evident. These findings may be the consequence of high prevalence of prenatal multivitamin and folate supplementation in this population (over 80%). It is therefore not surprising that folate deficiency may be rare and that the RFC-1 c.80A -> G polymorphism is less biologically significant for placental abruption.