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

Jeffrey C. Livingston, John R. Barton, Vicki Park, Bassam Haddad, Owen Phillips, Baha M. Sibai

Research output: Contribution to journalArticle

140 Citations (Scopus)

Abstract

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. STUDY DESIGN: 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 X2 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/667FFT 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). CONCLUSION: Inherited thrombophilias are not associated with severe preeclampsia.

Original languageEnglish (US)
Pages (from-to)153-157
Number of pages5
JournalAmerican Journal of Obstetrics and Gynecology
Volume185
Issue number1
DOIs
StatePublished - Jan 1 2001

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Pre-Eclampsia
Mothers
Prothrombin
Mutation
Genotype
Polymerase Chain Reaction
Eclampsia
Genetic Polymorphisms
Enzymes
Fetal Development
Hemolysis
Platelet Count
Fetal Blood
Vascular Diseases
African Americans
Gestational Age
Electrophoresis
Leukocytes
Cross-Sectional Studies
Gels

All Science Journal Classification (ASJC) codes

  • Obstetrics and Gynecology

Cite this

Maternal and fetal inherited thrombophilias are not related to the development of severe preeclampsia. / Livingston, Jeffrey C.; Barton, John R.; Park, Vicki; Haddad, Bassam; Phillips, Owen; Sibai, Baha M.

In: American Journal of Obstetrics and Gynecology, Vol. 185, No. 1, 01.01.2001, p. 153-157.

Research output: Contribution to journalArticle

Livingston, Jeffrey C. ; Barton, John R. ; Park, Vicki ; Haddad, Bassam ; Phillips, Owen ; Sibai, Baha M. / Maternal and fetal inherited thrombophilias are not related to the development of severe preeclampsia. In: American Journal of Obstetrics and Gynecology. 2001 ; Vol. 185, No. 1. pp. 153-157.
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abstract = "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. STUDY DESIGN: 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 X2 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/667FFT 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). CONCLUSION: Inherited thrombophilias are not associated with severe preeclampsia.",
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AU - Sibai, Baha M.

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N2 - 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. STUDY DESIGN: 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 X2 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/667FFT 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). CONCLUSION: Inherited thrombophilias are not associated with severe preeclampsia.

AB - 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. STUDY DESIGN: 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 X2 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/667FFT 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). CONCLUSION: Inherited thrombophilias are not associated with severe preeclampsia.

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