Maternal and fetal inherited thrombophilias are not related to the development of severe preeclampsia

OBJECTIVE: Thrombotic vascular disease may predispose patients to the devel opment of preeclampsia. The purpose of this study was to determine whether maternal or fetal genotype frequencies-of the inherited thrombophilic gene mutations (factor V Leiden, methylenetetrahydrofolate, and prothrombin) are altered in severe preeclampsia. STUDY DESIGN: We performed a prospective cross-sectional study to compare t he maternal and fetal genotype frequencies of factor V Leiden, methylenetet rahydrofolate, and prothrombin. One hundred ten patients with severe preecl ampsia were matched for gestational age to 97 normotensive pregnancies. Umb ilical cord blood was obtained from 92 control patients and 75 patients wit h preeclampsia. Deoxyribonucleic acid was extracted from leukocytes and pol ymerase chain reaction was performed. Polymerase chain reaction products we re digested with the appropriate restriction enzyme and fractionated by gel electrophoresis. Genotype frequencies were calculated. Statistical signifi cance was determined by the chi (2) test. RESULTS: There were no significant differences between patients with severe preeclampsia and control patients regarding frequency of maternal factor V Leiden G/506/A mutation (4.4% vs 4.3%; P=.96), methyl- enetetrahydrofolate CC/667/TT mutation (9.6% vs 6.3%; P=.54), or prothrombin G/202.10/A mutati on (0% vs 1.1%; P=.92). In addition, no statistical difference could be fou nd between fetal thrombophilias and the development of preeclampsia. Findin gs were similar in both white (n = 47) and African American (n = 63) preecl amptic subsets. Moreover, there was no association between any of the mater nal or fetal genetic polymorphisms and the incidence of hemolysis, elevated liver enzymes, and low platelet count syndrome (n 21); eclampsia (n = 12); or intrauterine growth restriction (n = 9). CONCLUSION: Inherited thrombophilias are not associated with severe preecla mpsia.