Maternal and fetal inherited thrombophilias are not related to the development of severe preeclampsia.
OBJECTIVE
Thrombotic vascular disease may predispose patients to the development 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.


METHODS
We performed a prospective cross-sectional study to compare the maternal and fetal genotype frequencies of factor V Leiden, methylenetetrahydrofolate, and prothrombin. One hundred ten patients with severe preeclampsia were matched for gestational age to 97 normotensive pregnancies. Umbilical cord blood was obtained from 92 control patients and 75 patients with preeclampsia. Deoxyribonucleic acid was extracted from leukocytes and polymerase chain reaction was performed. Polymerase chain reaction products were digested with the appropriate restriction enzyme and fractionated by gel electrophoresis. Genotype frequencies were calculated. Statistical significance 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), methylenetetrahydrofolate CC/667/TT mutation (9.6% vs 6.3%; P =.54), or prothrombin G/20210/A mutation (0% vs 1.1%; P =.92). In addition, no statistical difference could be found between fetal thrombophilias and the development of preeclampsia. Findings were similar in both white (n = 47) and African American (n = 63) preeclamptic subsets. Moreover, there was no association between any of the maternal 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).


CONCLUSIONS
Inherited thrombophilias are not associated with severe preeclampsia.
Livingston
J C
JC
Department of Maternal-Fetal Medicine, University of Tennessee, Memphis, TN, USA.
Barton
J R
JR
Park
V
V
Haddad
B
B
Phillips
O
O
Sibai
B M
BM
D000328:Adult; D003430:Cross-Sectional Studies; D004247:DNA / Q000097:blood; D005165:Factor V / Q000235:genetics; D005260:Female; D005312:Fetal Blood / Q000737:chemistry; D005315:Fetal Diseases / Q000235:genetics*; D005317:Fetal Growth Retardation / Q000235:genetics; D005787:Gene Frequency; D005838:Genotype; D005865:Gestational Age; D017359:HELLP Syndrome / Q000235:genetics; D006461:Hemolysis; D006801:Humans; D007962:Leukocytes / Q000737:chemistry; D042965:Methylenetetrahydrofolate Reductase (NADPH2); D009154:Mutation; D000587:Oxidoreductases Acting on CH-NH Group Donors / Q000235:genetics; D010976:Platelet Count; D016133:Polymerase Chain Reaction; D011225:Pre-Eclampsia / Q000235:genetics*; D011247:Pregnancy; D011446:Prospective Studies; D011516:Prothrombin / Q000235:genetics; D019851:Thrombophilia / Q000235:genetics*
C095381:factor V Leiden; D005165:Factor V; D011516:Prothrombin; D004247:DNA; D000587:Oxidoreductases Acting on CH-NH Group Donors; D042965:Methylenetetrahydrofolate Reductase (NADPH2)