Skip Navigation


QJM Advance Access originally published online on April 13, 2006
QJM 2006 99(5):289-298; doi:10.1093/qjmed/hcl040
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
99/5/289    most recent
hcl040v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (8)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Nurk, E.
Right arrow Articles by Vollset, S.E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nurk, E.
Right arrow Articles by Vollset, S.E.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 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

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

E. Nurk1,3,, G.S. Tell1,3, H. Refsum2,4, P.M. Ueland2,3 and S.E. Vollset1,3

From the 1Department of Public Health and Primary Health Care, 2Institute of Medicine, Section of Pharmacology, 3LOCUS for Homocysteine and Related Vitamins, University of Bergen, Bergen, Norway and 4Department of Pharmacology, University of Oxford, Oxford, UK

Address correspondence to Dr E. Nurk, Sõpruse 12–3, Viiratsi, Viljandimaa 70101, Estonia. email: eha.nurk{at}gmail.com

Received 30 September 2005 and in revised form 12 March 2006

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.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.