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

Blood Coagul Fibrinolysis. 2004 Mar;15(2):139-47. doi: 10.1097/00001721-200403000-00005.

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 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, chi2 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, chi2 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, chi2 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.

MeSH terms

  • 3' Untranslated Regions
  • Abruptio Placentae / etiology
  • Adolescent
  • Adult
  • Alleles
  • Amino Acid Substitution
  • DNA Mutational Analysis
  • Ethnicity / genetics
  • Factor V / genetics*
  • Female
  • Fetal Death / etiology
  • Fetal Growth Retardation / etiology
  • Fibrinogen / analysis*
  • Fibrinogen / genetics
  • Genetic Predisposition to Disease
  • Humans
  • Methylenetetrahydrofolate Reductase (NADPH2) / genetics*
  • Middle Aged
  • Mutation, Missense
  • Placental Circulation* / genetics
  • Point Mutation
  • Polymorphism, Genetic
  • Pre-Eclampsia / etiology
  • Pregnancy
  • Pregnancy Complications, Cardiovascular / etiology*
  • Pregnancy Complications, Hematologic / etiology*
  • Prevalence
  • Prothrombin / genetics*
  • Thrombophilia / genetics*

Substances

  • 3' Untranslated Regions
  • factor V Leiden
  • Factor V
  • Prothrombin
  • Fibrinogen
  • Methylenetetrahydrofolate Reductase (NADPH2)