Author

W.Zarzour; E.Bakir; W.Herrmann

Published in

Damascus University Journal of Health Sciences, Volume 18, Issue 1, 2002

Abstract

Mild hyperhomocysteinemia, a risk factor for ischemic heart disease (coronary heart disease CAD) can be caused by disturbans of homocysteine metabolism. Methylenetetrahydrofolate reductase (MTHFR) catalysis of 5-methylenetetrahydrofolate, to methyl donor for homocysteine remethylation to methionin. A common mutation in MTHFR, an alanine-to- valine substitution, may contribute to mild hyperhomocysteinemia in coronary artery disease. To test this hypothesis, we studied 78 patients with CAD by mutation analysis. And measurements of plasma homocysteine and several vitamins (Folate, B12). The difference in the prevalence of the homozygous mutant genotype between the CAD patients (8.5%) and healthy subjects (12%) was not significant. However, individuals with homozygous mutant genotype had higher plasma homocysteine, particularly when plasma Folate was below the median value. The genetic environmental interaction is proposed to be a risk factor for CAD.

Link to read full paper

http://www.damascusuniversity.edu.sy/mag/health/old/medical/2002/18-1/zarzour.pdf