Livingston J C, Barton J R, Park V, Haddad B, Phillips O, Sibai B M
Department of Maternal-Fetal Medicine, University of Tennessee, Memphis, TN, USA.
Am J Obstet Gynecol. 2001 Jul;185(1):153-7. doi: 10.1067/mob.2001.114691.
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.
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.
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).
Inherited thrombophilias are not associated with severe preeclampsia.
血栓性血管疾病可能使患者易患先兆子痫。本研究的目的是确定遗传性血栓形成倾向基因突变(因子V莱顿突变、亚甲基四氢叶酸还原酶突变和凝血酶原突变)的母体或胎儿基因型频率在重度先兆子痫中是否发生改变。
我们进行了一项前瞻性横断面研究,以比较因子V莱顿突变、亚甲基四氢叶酸还原酶突变和凝血酶原突变的母体和胎儿基因型频率。110例重度先兆子痫患者按孕周与97例血压正常的孕妇进行匹配。从92例对照患者和75例先兆子痫患者中获取脐带血。从白细胞中提取脱氧核糖核酸并进行聚合酶链反应。聚合酶链反应产物用适当的限制性内切酶消化,然后通过凝胶电泳进行分离。计算基因型频率。通过卡方检验确定统计学意义。
重度先兆子痫患者与对照患者在母体因子V莱顿G/506/A突变频率(4.4%对4.3%;P = 0.96)、亚甲基四氢叶酸还原酶CC/667/TT突变频率(9.6%对6.3%;P = 0.54)或凝血酶原G/20210/A突变频率(0%对1.1%;P = 0.92)方面无显著差异。此外,胎儿血栓形成倾向与先兆子痫的发生之间未发现统计学差异。在白人(n = 47)和非裔美国人(n = 63)先兆子痫亚组中的结果相似。此外,母体或胎儿的任何基因多态性与溶血、肝酶升高和血小板计数低综合征(n = 21)、子痫(n = 12)或胎儿生长受限(n = 9)的发生率之间均无关联。
遗传性血栓形成倾向与重度先兆子痫无关。