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Am J Obstet Gynecol. 2006 Jan;194(1):218-24.

Congenital heart defects, maternal homocysteine, smoking, and the 677 C>T polymorphism in the methylenetetrahydrofolate reductase gene: evaluating gene-environment interactions.

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  • 1Department of Pediatrics, Arkansas Children's Hospital Research Institute, University of Arkansas for Medical Sciences, College of Medicine, Little Rock, AR, USA.

Abstract

OBJECTIVE:

This study was undertaken to investigate the association between congenital heart defects (CHD), and maternal homocysteine, smoking, and the MTHFR 677 C>T polymorphism.

STUDY DESIGN:

Plasma homocysteine concentrations, smoking status, and MTFHR 677 genotypes were determined in 275 white women who had pregnancies affected by CHDs and 118 white women who had a normal pregnancy.

RESULTS:

Homocysteine concentrations were significantly higher among women who had affected pregnancies (P < .0001). The highest estimated risk for having a CHD-affected pregnancy was among women who were smokers, were in the highest quartile for homocysteine, and had the MTHFR 677 CC genotype (odds ratio [OR] 11.8; 95% CI 2.6-53.3).

CONCLUSION:

Many CHDs are due to a complex interaction between lifestyle factors and genetic susceptibilities. Our results suggest that the combined effect of elevations in maternal homocysteine, smoking, and the MTHFR 677 C>T polymorphism increase the risk of having a CHD-affected pregnancy.

PMID:
16389035
[PubMed - indexed for MEDLINE]
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