Journal
JOURNAL OF THROMBOSIS AND HAEMOSTASIS
Volume 2, Issue 9, Pages 1588-1593Publisher
WILEY
DOI: 10.1111/j.1538-7836.2004.00861.x
Keywords
factor V leiden; factor XIII; hereditary coagulation abnormalities; methylenetetrahydrofolate reductase (MTHFR); plasminogen activator inhibitor type (PAI)-1; preeclampsia; prothrombin; thrombin activatable fibrinolysis; inhibitor (TAFI)
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Recently, it has been proposed that abnormalities in coagulation and fibrinolysis contribute to the development of preeclampsia by increasing the thrombotic tendency. This hypothesis was tested in women who have had preeclampsia (cases) compared with matched controls. Polymorphisms in the thrombophilia genes {plasminogen activator inhibitor type 1 [PAI-1-675(4G/5G)], thrombin activatable fibrimolysis inhibitor (TAFI-438G/A and 1040C/T), methylenetetrahydrofolate reductase (MTHFR 677C/T), factor V (FV Leiden R/Q506), prothrombin (FII 20210G/A) and factor XIIIA (FXIIIA V/L34)} were determined in 157 women with preeclampsia and 157 women with uncomplicated pregnancy. The associated risk of preeclampsia was analyzed using logistic regression methods. The frequency distributions of the genotypes of these six polymorphisms in thrombophilia genes were similar in the case and control groups. We found no differences in the prevalence of genetic risk factors of thrombosis in women with preeclampsia compared with controls, which makes it unlikely that these polymorphisms are risk factors for preeclampsia.
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