THE FACTOR-V LEIDEN MUTATION MAY PREDISPOSE WOMEN TO SEVERE PREECLAMPSIA

OBJECTIVE: A recent study showed that resistance to activated protein C may underlie some cases of severe preeclampsia. A common missense mu tation in the factor V gene, the Leiden mutation, is the most frequent genetic cause of resistance to activated protein G. Our objective was to determine whether this mutation is more prevalent in patients with severe preeclampsia than in normotensive controls. STUDY DESIGN: Deox yribonucleic acid was extracted from whole blood of 158 gravid women m eeting criteria of The American College of Obstetricians and Gynecolog ists for severe preeclampsia and 403 normotensive gravid women. The po lymerase chain reaction was used to amplify exon 10 of the factor V ge ne, followed by allele-specific restriction with Mnl 1 for mutation de tection. Results were analyzed with a chi(2) contingency table. RESULT S: No patients were homozygous for the Leiden mutation. Fourteen of 15 8 women with severe preeclampsia (8.9%) were heterozygous for the Leid en mutation compared with 17 of 403 normotensive gravid controls (4.2% ). The difference in frequency between women with severe preeclampsia and normotensive controls was statistically significant, chi(2) 4.686, p = 0.03. CONCLUSIONS: Our data suggest that carriers of the factor V Leiden mutation are at increased risk for severe preeclampsia. Deoxyr ibonucleic acid analysis for the factor V Leiden mutation could serve as one component of a genetic screening profile for preeclampsia and o ther adverse pregnancy outcomes. Women who carry this mutation are at increased risk for deep venous thrombosis. Carriers of this common thr ombophilic mutation may be identified so that adequate counseling rega rding future contraceptive usage and effective thromboembolic prophyla xis during pregnancy and surgical procedures may be offered.