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QJM Advance Access published online on April 13, 2006
QJM, doi:10.1093/qjmed/hcl040
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© The Author 2006. Published by Oxford University Press on behalf of the Association of Physicians. All rights reserved. For Permissions, please email: Journals.permissions@oxfordjournals.org
Received September 30, 2005
Accepted March 12, 2006

Original Papers

Factor V Leiden, pregnancy complications and adverse outcomes: the Hordaland Homocysteine Study

E. Nurk 1 *, G.S. Tell 1, H. Refsum 2, P.M. Ueland 3, and S.E. Vollset 1

1 From the Department of Public Health and Primary Health Care, University of Bergen, Bergen, Norway; From the LOCUS for Homocysteine and Related Vitamins, University of Bergen, Bergen, Norway
2 From the Institute of Medicine, Section of Pharmacology, University of Bergen, Bergen, Norway; From the Department of Pharmacology, University of Oxford, Oxford, UK
3 From the Institute of Medicine, Section of Pharmacology, University of Bergen, Bergen, Norway; From the LOCUS for Homocysteine and Related Vitamins, University of Bergen, Bergen, Norway

* To whom correspondence should be addressed.
E. Nurk, E-mail: eha.nurk{at}gmail.com


  Abstract

Background: The factor V Leiden (FVL) mutation is the most common cause of inherited thrombophilia in Caucasian populations, and women with this variant allele are at increased risk for pregnancy complications.

Aim: To examine whether the FVL allele is associated with pregnancy complications and adverse outcomes in a population-based study, and to identify potential factors that interact with the FVL genotype.

Design: Retrospective cohort study in a geographically-defined area.

Methods: Polymorphisms of factor V 1691G->A, methylenetetrahydrofolate reductase (MTHFR) 677C -> T and 1298A -> C and plasma levels of total homocysteine, folate and vitamin B12 were determined in blood samples collected in 1992-1993 from 5874 women aged 40-42 years, and linked with 14 474 pregnancies in the same women, recorded in the Medical Birth Registry of Norway, 1967-1996.

Results: The allelic frequency of FVL was 3.7% (6.9% heterozygotes, 0.3% homozygotes). Maternal FVL mutation was associated with significantly higher risks of pre-eclampsia (OR 1.63, 95%CI 1.15-2.30), pre-eclampsia at <37 weeks (OR 2.76, 1.34-5.70), low birth weight (OR 1.34, 95%CI 1.03-1.74) and stillbirth (OR 2.20, 95%CI 1.45-3.36). The presence of a variant allele for the 677C -> T MTHFR polymorphism strengthened the association between FVL and stillbirth (OR 3.34, 95%CI 1.95-5.73) (pinteraction = 0.034).

Discussion: FVL mutation is a significant risk factor for pregnancy complications and adverse outcomes, and MTHFR 677CT/TT genotype can further enhance the risk of stillbirth.


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