Thrombophilic polymorphisms--factor V Leiden, prothrombin G20210A, and methylenetetrahydrofolate reductase C677T mutations--and preterm birth

Wien Klin Wochenschr. 2004 Sep 30;116(17-18):622-6. doi: 10.1007/s00508-004-0223-9.

Abstract

Aim of the study: To evaluate the influence of three common thrombophilic polymorphisms, factor V Leiden (FV), prothrombin G20210A (PT), and methylenetetrahydrofolate reductase (MTHFR) C677T mutations, on preterm birth of unknown cause.

Patients and methods: A single-centre case-control study of women with preterm infants < or =35 weeks of gestation, in whom obvious maternal, uterine, and fetal causes responsible for preterm birth were excluded (n = 35). The controls were 54 women with term infants hospitalised in the same ward.

Results: There were no significant differences between the groups of mothers in history of fetal loss, venous or familial thrombosis, or previous preterm birth. FV was found in 8.6% of the cases, PT in 5.7%, and MTHFR mutation (homozygous) in 4.8% compared with 5.4% (p=0.292, OR 1.594, CI95% 0.303-8.384), 7.4% (p=0.379, OR 0.758, CI95% 0.131-4.374), and 4.5% (p = 0.485, OR 1.050, CI95% 0.090-12.276), respectively, in the controls. Differences in the three thrombophilic polymorphisms in the two groups of infants were also not significant.

Conclusion: We could not demonstrate a distinct association between these thrombophilic polymorphisms and preterm birth.

Publication types

  • Comparative Study
  • Evaluation Study

MeSH terms

  • Adolescent
  • Adult
  • Case-Control Studies
  • Factor V / genetics*
  • Female
  • Gestational Age
  • Heterozygote
  • Homozygote
  • Humans
  • Infant, Newborn
  • Maternal Age
  • Methylenetetrahydrofolate Reductase (NADPH2) / genetics*
  • Mutation
  • Odds Ratio
  • Polymorphism, Genetic*
  • Pregnancy
  • Premature Birth / genetics*
  • Prothrombin / genetics*
  • Thrombophilia / genetics*

Substances

  • factor V Leiden
  • Factor V
  • Prothrombin
  • Methylenetetrahydrofolate Reductase (NADPH2)