Factor V Leiden, prothrombin G20210A, and methylene tetrahydrofolate reductase mutations and stillbirth: the Stillbirth Collaborative Research Network

详细信息    查看全文

• 作者：Robert M. Silver ; MD^a ; ^{bsilver@hsc.utah.edu" class="auth_mail" title="E-mail the corresponding author} ; George R. Saade ; MD^b ; Vanessa Thorsten ; BA^d ; Corette B. Parker ; DrPH^d ; Uma M. Reddy ; MD ; MPH^e ; Carey Drews-Botsch ; PhD^f ; Deborah Conway ; MD^c ; Donald Coustan ; MD^h ; Donald J. Dudley ; MD^c ; Radek Bukowski ; MD ; PhD^b ; Carol J. Rowland Hogue ; PhD^g ; Halit Pinar ; MD^h ; Michael W. Varner ; MD^a ; Robert Goldenberg ; MDⁱ ; Marian Willinger ; PhD^e
• 关键词：placenta ; stillbirth ; thrombophilia
• 刊名：American Journal of Obstetrics and Gynecology
• 出版年：2016
• 出版时间：October 2016
• 年：2016
• 卷：215
• 期：4
• 页码：468.e1-468.e17
• 全文大小：418 K

文摘

An evaluation for heritable thrombophilias is recommended in the evaluation of stillbirth. However, the association between thrombophilias and stillbirth remains uncertain.

bsSec_2">Objective

bspara0015">We sought to assess the association between maternal and fetal/placental heritable thrombophilias and stillbirth in a population-based, case-control study in a geographically, racially, and ethnically diverse population.

bsSec_3">Study Design

bspara0020">We conducted secondary analysis of data from the Stillbirth Collaborative Research Network, a population-based case-control study of stillbirth. Testing for factor V Leiden, prothrombin G20210A, methylene tetrahydrofolate reductase C677T and A1298C, and plasminogen activating inhibitor (PAI)-1 4G/5G mutations was done on maternal and fetal (or placental) DNA from singleton pregnancies. Data analyses were weighted for oversampling and other aspects of the design. Odds ratios (OR) were generated from univariate models regressing stillbirth/live birth status on each thrombophilia marker.

bsSec_4">Results

bspara0025">Results were available for ≥1 marker in 488 stillbirths and 1342 live birth mothers and 405 stillbirths and 990 live birth fetuses. There was an increased odds of stillbirth for maternal homozygous factor V Leiden mutation (2/488; 0.4% vs 1/1380; 0.0046%; OR, 87.44; 95% confidence interval, 7.88–970.92). However, there were no significant differences in the odds of stillbirth for any other maternal thrombophilia, even after stratified analyses. Fetal 4G/4G PAI-1 (OR, 0.63; 95% confidence interval, 0.43–0.91) was associated with decreased odds of stillbirth. Other fetal thrombophilias were similar among groups.

bsSec_5">Conclusion

bspara0030">Most maternal and fetal thrombophilias were not associated with stillbirth. Maternal factor V Leiden was weakly associated with stillbirth, and the fetal PAI-1 4G/4G polymorphism was associated with live birth. Our data do not support routine testing for heritable thrombophilias as part of an evaluation for possible causes of stillbirth.