Objective: To examine the prevalence of maternal thrombophilia in women wit
h severe preeclampsia/eclampsia, placental abruption, fetal growth restrict
ion, and unexplained stillbirth.
Methods: We studied 102 women who had pregnancy complications and 44 health
y women with uncomplicated pregnancies. All women were tested 10 weeks post
partum for mutations of factor V Leiden, methylenetetrahydrofolate reductas
e (MTHFR) C677T, and G20210A prothrombin gene; deficiencies of protein C, p
rotein S, and antithrombin III; and the presence of lupus anticoagulant and
anticardiolipin antibodies. We aimed to recruit 100 cases and 300 controls
to detect a 10% difference in thrombophilia between the groups. However, w
e were able to recruit only 44 controls.
Results: Abnormal thrombophilia screen was found in 54 women with pregnancy
complications (53%) and in 17 women (39%) with normal pregnancies (odds ra
tio [OR] 1.8; 95% confidence interval [CI] 0.87, 3.67). Mutations encoding
for factor V Leiden, G20210A prothrombin gene, and MTHFR C677T (homozygous)
were identified in 18% of women with complications compared with 16% of co
ntrols (OR 1.1; 95% CI 0.44, 2.94). Activated protein C resistance, not due
to factor V Leiden mutation, was the most common thrombophilic defect, fou
nd in 26% of women with pregnancy complications compared with 18% of contro
ls (OR 1.5; 95% CI 0.63, 3.73). Twenty women with complications (20%) had m
ultiple thrombophilic defects compared with four controls (9%) (OR 2.4; 95%
CI 0.78, 7.61).
Conclusion: In our cohort of women with pregnancy complications, maternal t
hrombophilia was less common than previously thought, and multiple thrombop
hilias were not a major additional risk factor. (Obstet Gynecol 2001;97: 75
3-9. (C) 2001 by The American College of Obstetricians and Gynecologists.).