0505 for CAD patients and P = 0.262 for healthy controls). The genotype distribution of IL-6-174G>C polymorphism in CAD patients showed a significant difference among the patients and control subjects (P = 0.0025; P value from 3 �� 2 contingency table). The IL-6-174C variant allele selleck chem inhibitor was more prevalent in 34.7% patients compared with 13.5% in control subjects. There was a significant difference between the C and G allele frequencies in CAD cases and controls (OR = 3.4, 95% CI = 1.53�C7.70, P = 0.0015, Table 2). The relationships of -174G>C polymorphism on serum IL-6 and hs-CRP levels are shown in Figure 2. Mean serum IL-6 and hs-CRP levels varied significantly among the IL-6 promoter genotypes within patient group. Carriers of CC genotype showed the highest levels of serum IL-6 and hs-CRP when compare with GC and GG genotypes (P < 0.

0001, and P < 0.0001, resp., Figure 2). Binary logistic regression analysis for possible association of CAD with age, BMI, serum IL-6, serum hs-CRP, and -174G>C polymorphism is shown in Table 3. Four variables age (P = 0.008), serum IL-6 (P = 0.008), serum hs-CRP (P < 0.0001), and the -174G>C polymorphism (P = 0.029) were significantly associated with cardiovascular disease phenotype.Figure 2Influence of IL-6-174G>C polymorphism on the circulating levels of IL-6 and hsCRP in cardiovascular disease patients. Data represent mean �� SE. (a) Serum IL-6 levels, P < 0.0001, (b) serum hsCRP levels (P < 0.0001), in ...Table 2IL-6-174G>C genotype and allele frequencies of study population n = 88.Table 3Binary logistic regression analysis in all subjects when CVD was taken as a response variable.

4. Discussion Although there is increasing evidence related to a central role of IL-6 in orchestrating the inflammatory cascades resulting in pathophysiology of CAD, the genetic regulation of its expression has been found to be complex. Several researchers have reported a potential influence of promoter polymorphisms on regulation of IL-6 at transcriptional level. But studies based on case-control association of -174G>C polymorphism with coronary events have shown conflicting results. To our knowledge there is no data available on genetic regulation of IL-6 in CAD patients in our population. Therefore, we questioned the association between CVD evidence and -174G>C polymorphism along with circulating IL-6 and hs-CRP levels in high-risk native Pakistani families.

In the current study, IL-6 promoter region polymorphism was significantly associated with CAD, and this association remained significant in multivariate analysis, even in the presence of confounding variables. Minor allele C at -174G>C was more prevalent (34.7%) Entinostat in patients compared with healthy subjects (13.5%). Previous studies based on association of this polymorphism with different phenotypes of CAD have produced discrepant results.