Vol. 79, December 2011

Frequency of Thrombotic Gene Mutations in Diabetic Patients with and Without Coronary Artery Disease

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Frequency of Thrombotic Gene Mutations in Diabetic Patients with and Without Coronary Artery Disease,OLFAT M. HENDY, ELHAMY ABD AL MONEAM, MAHA ALLAM, SOMAYH SOLIMAN, AMANY KAMAL and GAMAL ABD EL NASSER

 

Abstract
Although relationship between diabetic atherogenesis and several common risk factors plus non traditional risk markers have been studied extensively and the data is having some controversies. This study aimed to find the relationship between factor V Leiden, prothrombin G20210A and methylene tet-rahydrofolate reductase (MTHFR) gene mutations and occur-rence of coronary artery disease (CAD) in diabetic patients and to compare with healthy controls. 72 diabetic patients, 29 of them have proven CAD and the remaining 43 have not. Twenty healthy subjects were included in the study as a control group. All patients and controls were subjected to history, physical examination and Electrocardiography. Routine labo-ratory investigations, as well as plasma homocysteine were done. Factor V G1691A, prothrombin G20210A (PTHR A20210) and MTHFR C677—>T genotypes were determined by polymerase chain reaction using the commercial throm-botype test. The prevalence's of heterozygotes for F V G1691 A and F II G20210A were not significantly different between both patient groups (6.9% versus 6.8% and 2.3% versus 3.4% among DM without and CAD, respectively), however, no cases were found among control group as regard two poly-morphisms. In contrast, the prevalence of MTHFR C677—>T was significantly higher in CAD patients (23.3% versus 37.9% and 10% among CAD, DM and controls, respectively). There is a strong relationship between MTHFR C677—>T and presence of hypertension, hypercholesterolemia and hyperhomocys-teinemia.
In Conclusion: Diabetic patients with CAD have signifi-cantly higher MTHFR gene polymorphism as compared to diabetic patients with no CAD and the presented data suggest a synergistic effect between atherogenic and thrombogenic risk factors in the pathogenesis of CAD. Future study with a large scale population recommend to collaborate these poly-morphisms with other risk factors.

 

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