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-455G/A beta-fibrinogen gene polymorphism, factor V Leiden, prothrombin G20210A mutation and MTHFR C677T, and placental vascular complications

Camilleri, RS; Peebles, D; Portmann, C; Everington, T; Cohen, H; (2004) -455G/A beta-fibrinogen gene polymorphism, factor V Leiden, prothrombin G20210A mutation and MTHFR C677T, and placental vascular complications. BLOOD COAGUL FIBRIN , 15 (2) 139 - 147. 10.1097/01.mbc.0000114378.15192.1a.

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Abstract

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 tetra hydrofolate 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. (C) 2004 Lippincott Williams Wilkins.

Type: Article
Title: -455G/A beta-fibrinogen gene polymorphism, factor V Leiden, prothrombin G20210A mutation and MTHFR C677T, and placental vascular complications
DOI: 10.1097/01.mbc.0000114378.15192.1a
Keywords: -4556/A polymorphism, fibrinogen, obstetric complications, placenta, hereditary thrombophilic markers, CORONARY-HEART-DISEASE, CARDIOVASCULAR RISK-FACTORS, GLASGOW MONICA SURVEY, PLASMA-FIBRINOGEN, MYOCARDIAL-INFARCTION, FACTOR-VII, VENOUS THROMBOSIS, ALPHA-FIBRINOGEN, ARTERY-DISEASE, FETAL LOSS
UCL classification: UCL > Provost and Vice Provost Offices
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences > Cancer Institute
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Medical Sciences > Cancer Institute > Research Department of Haematology
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Pop Health Sciences > Inst for Women's Health
UCL > Provost and Vice Provost Offices > School of Life and Medical Sciences > Faculty of Pop Health Sciences > Inst for Women's Health > Maternal and Fetal Medicine
URI: http://discovery.ucl.ac.uk/id/eprint/114430
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