Interleukin-6-572C>G polymorphism—association with inflammatory variables in Korean men with coronary artery disease

Growing evidence suggests that polymorphisms at position −174 and −572 in interleukin-6 (IL-6) gene are associated with various manifestations of atherosclerosis. We investigated the genotype effects of IL-6 −174 and −572 polymorphisms on circulating levels of inflammatory markers in Korean men with coronary artery disease (CAD). CAD patients were subdivided into 2 groups; those patients treated without lipid-lowering drug (LLD) (n = 173) and those treated with LLD (n = 353). No significant differences existed between the 2 groups in age, body mass index, blood pressure, serum glucose, alcohol consumption, cigarette smoking, and the proportions of antihypertensive and antiplatelet therapies. IL-6 − 572 C>G polymorphism was only observed in this population. In CAD patients not taking LLD, the G/G genotype of the −572C>G polymorphism was associated with greater concentrations of IL-6 (C/C: 4.1 ± 0.8 pg/mL, C/G: 3.7 ± 0.7, G/G: 12.4 ± 6.6; P = 0.031), C-reactive protein (CRP) (C/C: 1.9 ± 0.4 mg/dL, C/G: 2.7 ± 0.8, G/G: 10.1 ± 3.9; P = 0.002), fibrinogen (C/C: 334 ± 6 mg/dL, C/G: 345 ± 13, G/G: 429 ± 38; P = 0.003), and oxidized low-density lipoprotein (ox-LDL) (C/C: 59 ± 2 mg/dL, C/G: 55 ± 3, G/G: 71 ± 6; P = 0.041) than those with C/C or C/G. However, in the LLD group, no difference existed in circulating levels of IL-6, CRP, fibrinogen, and ox-LDL across the genotype after adjustment of age. This study suggests that circulating levels of IL-6 and its related proteins such as CRP and fibrinogen are associated with genotype at a promoter polymorphism (−572C>G) of the IL-6 gene in Korean men with CAD not taking LLD. LLD, mostly statin in this study, might reduce the exaggeration of G/G genotype-raising effect on inflammatory markers.