|Title||–455G/A β-fibrinogen gene polymorphism, factor V Leiden, prothrombin G20210A mutation and MTHFR C677T, and placental vascular complications|
|Authors||Camilleri, R., Peebles, D., Portmann, C., Everington, T. and Cohen, H.|
Hyperfibrinogenaemia is associated with systemic arterial and venous thromboembolism and therefore may contribute to placental vascular disease associated with obstetric complications. The fibrinogen-raising -455G/A [beta]-fibrinogen gene polymorphism may enhance the physiological increase in fibrinogen levels during pregnancy and thereby predispose to obstetric complications. This retrospective case–control study looked at the association between the [beta]-fibrinogen gene polymorphism -455G/A, the hereditary thrombophilic markers factor V Leiden, prothrombin G20210A mutation (PGM) and C677T methylene tetrahydrofolate reductase (MTHFR), and obstetric complications associated with placental vascular disease. The study group (n = 247) comprised 147 women (90 Caucasian) who met the clinical criteria and a control group of 100 parous women (90 Caucasian) with no history of obstetric or medical complications. No significant differences were observed in the -455A allelic frequencies of the patient and normal control groups, with (allelic frequencies, 0.156 and 0.178, respectively; P = 0.5716, [chi]2 test, odds ratio = 1.17, 95% confidence interval = 0.65–2.13) or without (allelic frequencies, 0.129 and 0.170, respectively; P = 0.2077, [chi]2 test, odds ratio = 1.38, 95% confidence interval = 0.81–2.35) the exclusion of non-Caucasian women. There was an increased prevalence of factor V Leiden among Caucasian patients compared with normal controls (allelic frequencies, 0.056 and 0.017, respectively; P = 0.048, [chi]2 test, odds ratio = 0.29, 95% confidence interval = 0.05–1.15) but there were no differences in the prevalences of PGM or MTHFR. These data suggest that factor V Leiden is associated with an increased risk of obstetric complications, but that the -455A allele of [beta]-fibrinogen, PGM and MTHFR do not appear to be implicated.
|Journal||Blood Coagulation & Fibrinolysis|
|Journal citation||15 (2), pp. 139-147|
|Publisher||Lippincott Williams & Wilkins|