학술논문

Association between the 2756A> G variant in the gene encoding methionine synthase and myocardial infarction in Tunisian patients
Document Type
Clinical report
Source
Clinical Chemistry and Laboratory Medicine. Oct 1, 2008, Vol. 46 Issue 10, p1364, 5 p.
Subject
Tunisia
Language
English
ISSN
1434-6621
Abstract
Byline: Riadh Jemaa, Research Laboratory LAB-SM-01 and Department of Biochemistry, Rabta University Hospital, Tunis, Tunisia; Afef Achouri, Research Laboratory LAB-SM-01 and Department of Biochemistry, Rabta University Hospital, Tunis, Tunisia; Amani Kallel, Research Laboratory LAB-SM-01 and Department of Biochemistry, Rabta University Hospital, Tunis, Tunisia; Samir Ben Ali, Research Laboratory LAB-SM-01 and Department of Biochemistry, Rabta University Hospital, Tunis, Tunisia; Sami Mourali, Department of Cardiology, Rabta University Hospital, Tunis, Tunisia; Moncef Feki, Research Laboratory LAB-SM-01 and Department of Biochemistry, Rabta University Hospital, Tunis, Tunisia; Monia Elasmi, Research Laboratory LAB-SM-01 and Department of Biochemistry, Rabta University Hospital, Tunis, Tunisia; Samah Haj Taieb, Research Laboratory LAB-SM-01 and Department of Biochemistry, Rabta University Hospital, Tunis, Tunisia; Haifa Sanhaji, Research Laboratory LAB-SM-01 and Department of Biochemistry, Rabta University Hospital, Tunis, Tunisia; Souheil Omar, Research Laboratory LAB-SM-01 and Department of Biochemistry, Rabta University Hospital, Tunis, Tunisia; Rachid Mechmeche, Department of Cardiology, Rabta University Hospital, Tunis, Tunisia; Naziha Kaabachi, Research Laboratory LAB-SM-01 and Department of Biochemistry, Rabta University Hospital, Tunis, Tunisia Keywords: homocysteine, methionine synthase, MTR, myocardial infarction, polymorphism Abstract Background: Elevated plasma total homocysteine (tHcy), a risk factor for coronary artery disease (CAD), is due to defects in genes encoding for enzymes involved in tHcy metabolism or from inadequate status of vitamins involved in tHcy disposal. Methionine synthase (MS), a vitamin B.sub.12-dependent enzyme, catalyses the remethylation of homocysteine to methionine using a methyl group donated by 5-methyltetra-hydrofolate, which is the major circulating form of folate in the body. Functional genetic variants of the MS may alter tHcy as well as folate levels which are independent risk factors for CAD. The influence of a common genetic polymorphism 2756A>G of the MS gene (MTR) on plasma tHcy, folate and vitamin B.sub.12 levels and its relation to the risk of myocardial infarction (MI) in a Tunisian case-control study was investigated. Methods: A total of 321 Tunisian patients with MI and 343 healthy controls were included in the study. The 2756A>G variant of the MTR was determined by polymerase chain reaction-restriction fragment length polymorphism analysis. Plasma tHcy was assessed with a fluorescent polarising immunoassay method. Plasma vitamin B.sub.12 and folate were determined by microparticular enzyme immunoassay and ion-capture, respectively. Results: A significant difference in genotype distribution and allele frequency was observed between patients and controls. Patients with MI had a frequency of 1.9% for the GG genotype, 26.2% for the AG genotype and 72% for the AA genotype. Controls had a frequency of only 0.9% for the GG genotype, 18.7% for the AG genotype and 80.5% for the AA genotype ([chi].sup.2=6.97, p=0.03). The MI patient group showed a significant higher frequency of the G allele compared to controls (0.149 vs. 0.101; OR 1.55; 95% CI 1.10-2.18; p=0.008). The association between the 2756A>G variant in the gene encoding MS and MI was no longer significant after adjustment for other well-established risk factors. When clinical and laboratory values were compared amongst genotypes in the study groups, no significant differences were noted. Conclusions: The present study showed a significant but not independent association between the 2756A>G polymorphism of the MTR (presence of G allele) and MI in the Tunisian population. Clin Chem Lab Med 2008; 46:1364-8. Article History: Date received: January 24, 2008 Date accepted: July 6, 2008 Author Notes: Corresponding author: Dr. Riadh Jemaa, Laboratoire de Biochimie, Hopital la Rabta, 1007, Jabbari, Tunis, Tunisia Phone: +216-71-561-912/98-819-168, Fax: +216-71-561-912, Email: jemaa_riadh@yahoo.fr