Jančić, Ivan (24721867100)Ivan (24721867100)JančićArsenović-Ranin, Nevena (59662809600)Nevena (59662809600)Arsenović-RaninŠefik-Bukilica, Mirjana (8118591400)Mirjana (8118591400)Šefik-BukilicaŽivojinović, Sladjana (35754184300)Sladjana (35754184300)ŽivojinovićDamjanov, Nemanja (8503557800)Nemanja (8503557800)DamjanovSpasovski, Vesna (26655022200)Vesna (26655022200)SpasovskiSrzentić, Sanja (57204289670)Sanja (57204289670)SrzentićStanković, Biljana (35785023700)Biljana (35785023700)StankovićPavlović, Sonja (7006514877)Sonja (7006514877)Pavlović2025-06-122025-06-122013https://doi.org/10.1007/s00296-012-2586-yhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-84878678926&doi=10.1007%2fs00296-012-2586-y&partnerID=40&md5=c334b645419ffe0bbe09614de3177bfahttps://remedy.med.bg.ac.rs/handle/123456789/9138To examine whether -174G/C interleukin-6 (IL-6) gene polymorphism, previously reported to correlate with IL-6 level, influences response to etanercept therapy in patients with rheumatoid arthritis. Seventy-seven patients with active RA were studied, at baseline and 6- and 12-month follow-up after etanercept therapy. Treatment response was estimated according to the European League Against Rheumatism response criteria. RA patients were genotyped for -174G/C IL-6 gene polymorphism by the PCR-RFLP method, and influence of genotype at this polymorphism to clinical response to etanercept was assessed. After 12 months of treatment, the percentage of responders (patients who had DAS28 improvement >1.2) was significantly increased in patients carrying the IL-6 -174G/G genotype (95.7 %) compared with those with the G/C (75.6 %) or CC (44.4 %) genotype (p = 0.006 by Chi-square test). No significant difference in the mean values of DAS28 improvement was observed between groups with different genotype. RA patients with an IL-6 -174GG genotype respond to etanercept better than patients with GC or CC genotype. This finding, if confirmed in future studies, suggests that the -174G/C IL-6 polymorphism may be a genetic marker of responsiveness to tumor necrosis factor-alpha (TNF-α) blockers in RA. © 2012 Springer-Verlag Berlin Heidelberg.-174G/C IL-6 polymorphismDAS28 improvementEtanerceptRheumatoid arthritis