-455G/A beta-fibrinogen gene polymorphism, factor V Leiden, prothrombin G20210A mutation and MTHFR C677T, and placental vascular complications.
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.
Camilleri
Raymond S
RS
Haemostasis Research Unit, Department of Haematology, University College London School of Medicine, University College London Hospitals NHS Trust, London, UK. r.camilleri@ucl.ac.uk
Peebles
Donald
D
Portmann
Carol
C
Everington
Tamara
T
Cohen
Hannah
H
D020413:3' Untranslated Regions; D000037:Abruptio Placentae / Q000209:etiology; D000293:Adolescent; D000328:Adult; D000483:Alleles; D019943:Amino Acid Substitution; D004252:DNA Mutational Analysis; D005006:Ethnicity / Q000235:genetics; D005165:Factor V / Q000235:genetics*; D005260:Female; D005313:Fetal Death / Q000209:etiology; D005317:Fetal Growth Retardation / Q000209:etiology; D005340:Fibrinogen / Q000032:analysis* / Q000235:genetics; D020022:Genetic Predisposition to Disease; D006801:Humans; D042965:Methylenetetrahydrofolate Reductase (NADPH2) / Q000235:genetics*; D008875:Middle Aged; D020125:Mutation, Missense; D021041:Placental Circulation / Q000235:genetics; D017354:Point Mutation; D011110:Polymorphism, Genetic; D011225:Pre-Eclampsia / Q000209:etiology; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000209:etiology*; D011250:Pregnancy Complications, Hematologic / Q000209:etiology*; D015995:Prevalence; D011516:Prothrombin / Q000235:genetics*; D019851:Thrombophilia / Q000235:genetics*
D020413:3' Untranslated Regions; C095381:factor V Leiden; D005165:Factor V; D011516:Prothrombin; D005340:Fibrinogen; D042965:Methylenetetrahydrofolate Reductase (NADPH2)