Preeclampsia and its interaction with common variants in thrombophilia genes

J Thromb Haemost. 2004 Sep;2(9):1588-93. doi: 10.1111/j.1538-7836.2004.00861.x.

Abstract

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 fibrinolysis 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.

MeSH terms

  • Adult
  • Carboxypeptidase B2 / genetics
  • Case-Control Studies
  • Factor V / genetics
  • Factor XIIIa / genetics
  • Female
  • Genetic Variation
  • Humans
  • Methylenetetrahydrofolate Reductase (NADPH2) / genetics
  • Plasminogen Activator Inhibitor 1 / genetics
  • Polymorphism, Genetic
  • Pre-Eclampsia / blood
  • Pre-Eclampsia / etiology*
  • Pre-Eclampsia / genetics*
  • Pregnancy
  • Prothrombin / genetics
  • Thrombophilia / blood
  • Thrombophilia / complications*
  • Thrombophilia / genetics*

Substances

  • Plasminogen Activator Inhibitor 1
  • factor V Leiden
  • Factor V
  • Prothrombin
  • Methylenetetrahydrofolate Reductase (NADPH2)
  • Factor XIIIa
  • Carboxypeptidase B2