For example, Kahn and coworkers (2009) found no higher risk for early-onset or severe preeclampsia in women with factor V Leiden mutation, prothrombin G20210A mutation, MTHFR C677T polymorphism, or hyperhomocysteinemia. Said and associates (201 Oa) prospectively screened more than 2000 healthy nulliparous women for factor V Leiden, prothrombin
Protein C deficiency 2.29 NA NA 3.05 5.15 NA (0.20-26.43) (0.24-38.51) (0.26-102.22) (0.23-151.58)
Protein 5 deficiency 3.55 NA NA 20.09 2.83 2.1o1 NA (0.35-35.72) (3.70-109.1•5) (0.76-10.57) (0.47-9.34)
Anticardiolipin 3.40 5.05 NA 3.30 2.73 1.42 6.91 antibodies (1.33-8.68) (1.82-14.01 ) (1.62-6.70) (1.65-4.51 ) (0.42-4.77) (2.70-1•7.68)
Lupus anticoagulants 2.97 NA 14.28 2.38 1.45 NA NA (nonspecific (1.03-9.76) (4.72-43.20) (0.81-6.98) (0.70-4.61)
Hyper-6.25 4.21 NA 0.98 3.49 2.40 NA homocysteinemia (1.37-28.42) (1.28-13.87) (0.1o7-5.55) (1.21-10.1•1) (0.36-15.89)
Homozygous and heterozygous carriers were grouped together; it is not possible to extract data for each state.
Data are presented as odds ratio (OR [95% CI]) and are derived from Robertson, 2005. Bolded numbers are statistically significant.
MTHFR = methylene tetrahydrofolate reductase variant; NA = not available.
Reproduced with permission from Bates 5M, Greer iA, Middledorp 5, et al: TE, thrombophilia, antithrombotic therapy, and pregnancy.
Chest 141 :e691 5,201o2.
gene mutation, MTHFR C677T, MTHFR A1298C, and thrombomodulin polymorphism. Women who carried the prothrombin gene mutation had a 3.6-fold greater risk of adverse pregnancy outcome, including severe preeclampsia, fetal-growth restriction, placental abruption, or stillbirth. But, none of the other polymorphisms conferred an elevated risk of these adverse outcomes. From the Stillbirth Collaborative Research Network, Silver and associates (2016) found a weak association between maternal factor V Leiden and stillbirth. here was no association between stillbirth and the other inherited thrombophilias. Based on their prospective study of 750 pregnancies complicated by stillbirth, Korteweg and colleagues (2010) concluded that routine thrombophilia testing after fetal death is inadvisable.