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Background: Coronary artery disease (CAD) is a multifactorial disorder. It is important to identify gene mutations that may be responsible for the development of CAD. The aim of this study was to determine the frequency of twelve cardiovascular disease (CVD) related gene mutations in coronary artery patients. Methods:The CVD StripAssay (Vienna Lab, Austria) was performed to analyze the twelve gene mutations on 52 coronary artery patients and 39 healthy controls. After DNA isolation from blood samples, hybridization with biotin marked probes was performed to PCR products containing the related region of mutant genes. Chisquare tests were used for statistical analyses.Results: Any differences were not observed between coronary artery patients and healthy controls in terms of the frequencies of studied twelve gene mutations except MTHFR A1298C mutation. It was observed that heterozygous and homozygous mutant genotypes of MTHFR A1298C mutation have protective effects against coronary artery disease [p = 0.06, in 95% CI OR = 0.205 (0.0421-1.001)]. Although all the three genotypes of PAI-1 4G/5G, ACE I/D and MTHFR C677T mutations were observed in both groups; homozygous mutant genotypes weren't observed for the Factor V Leiden, Factor V H1299R, Prothrombin G20210A, Factor XIII V34L, β-Fibrinojen -455G > A, HPA-1 1a/1b mutations in any of the groups. Heterozygote and homozygote mutant genotypes of APOB R3500Q mutation was not seen in both groups. When the patient group was evaluated in terms of compound genotypes, the rate of two mutations (ACE I/D, MTHFR A1298C) was 56%, the rate of three mutations (PAI-1 4G/5G, MTHFR A1298C, ACE I/D) was 53%, the rate of four mutations (PAI-1 4G/5G, MTHFR A1298C, HPA-1 1a/1b, ACE I/D) was 33%. High cholesterol, the number of clogged arteries and smoking rates was high in CAD patients with compound genotypes or carrying mutations in multiple genes compared the others. Conclusion:Among 12 studied gene mutations, only the MTH-FR A1298C mutation was determined to have a protective effect against CAD. In addition, cumulative effects of the mutant genotypes and environmental factors on people with the combined genotypes may be trigger for CAD.

Background: Beta cell death by apoptosis is an important mechanism in beta cell dysfunction and development of diabetes. Inhibition of apoptosis may be helpful approach in the prevention of diabetes. In this context, non-invasive, specific markers are needed to detect apoptosis in prediabetic stage. In the present study serum levels of cytokeratin-18/M30 antigen, a surrogate marker of apoptosis were investigated in cases with type 2 diabetes and Impaired Glucose Tolerance (IGT).