The interactive role of type 2 diabetes mellitus and E-selectin S128R mutation on susceptibility to coronary heart disease
1 Genetics Department, King Faisal Specialist Hospital and Research Centre, Riyadh 11211, Saudi Arabia
2 Biological and Medical Research Department, King Faisal Specialist Hospital and Research Centre, Riyadh 11211, Saudi Arabia
3 Biostatistics, Epidemiology and Scientific Computing Department, King Faisal Specialist Hospital and Research Centre, Riyadh 11211, Saudi Arabia
BMC Medical Genetics 2007, 8:35 doi:10.1186/1471-2350-8-35Published: 20 June 2007
The role of gene-environment interactions as risk factors for coronary heart disease (CAD) remains largely undefined. Such interactions may involve gene mutations and disease conditions such as type 2 diabetes mellitus (DM2) predisposing individuals to acquiring the disease.
In the present study, we assessed the possible interactive effect of DM2 and E-selectin S128R polymorphism with respect to its predisposing individuals to CAD, using as a study model a population of 1,112 patients and 427 angiographed controls of Saudi origin. E-selectin genotyping was accomplished by polymerase chain reaction (PCR) amplification followed by PstI restriction enzyme digestion.
The results show that DM2 is an independent risk factor for CAD. In the absence of DM2, the presence of the R mutant allele alone is not significantly associated with CAD (p = 0.431, OR 1.28). In contrast, in the presence of DM2 and the S allele, the likelihood of an individual acquiring CAD is significant (odds ratio = 5.44; p = < 0.001). This effect of DM2 becomes remarkably greater in the presence of the mutant 128R allele, as can be observed from the odds ratio of their interaction term (odds ratio = 6.11; p = < 0.001).
Our findings indicate therefore that the risk of acquiring CAD in patients with DM2 increases significantly in the presence of the 128R mutant allele of the E-selectin gene.