Background Interleukin (IL)-6 is involved in the pathogenesis of rheumatoid arthritis (RA) via its broad effects on immune and inflammatory responses. Sustained IL-6 activity can cause tissue damage in different tissues. Previous studies have shown that G allele at the -174G >C (rs1800795) polymorphism is related to high producing IL-6.
Purpose The aim of our study was to explore the potential role of IL-6 genetic polymorphisms as a predictor of tocilizumab efficacy in RA patients and to compare the results with a previous GWAS.
Material and methods The IL-6 (G >C) (rs1800795) genetic variant was genotyped using predesigned TaqMan genotyping assay technology and analysed on a ViiA7 real time PCR system. Clinical response was evaluated at 24 weeks with the use of the 28 joint disease activity score criteria (DAS28) and good response and remission were classified according to EULAR criteria. EULAR good response was defined as a change in DAS28 >1.2 and DAS28 ≤3.2. EULAR remission was defined as DAS28 ≤2.6 at 14 weeks. Statistical analysis was performed using SPSS v.20
Results Clinical data for 140 tocilizumab treated patients were obtained. The patients were aged (mean±SD) 53.25 ± 12.42 years; 79% were female. Mean DAS28 at baseline was 5.71 ± 1.13. The IL-6 G >C genetic polymorphisms were not significantly associated with a good EULAR response (CC vs no CC p = 0.35, OR=1.07, 95% CI 0.05 to 19.7; GC vs no GC p = 0.97, OR=1.03, 95% CI 0.22 to 4.70; GG vs no GG p = 0.50, OR=0.58, 95% CI 0.12 to 2.67), or remission (CC vs no CC p = 0.85, OR=1.11, 95% CI 0.41 to 2.98; GC vs no GC p = 0.98, OR=1.01, 95% CI 0.52 to 1.94; GG vs no GG p = 0.88, OR=0.96, 95% CI 0.48 to 1.89).
Conclusion Our results confirm that IL-6 G >C rs 1800795 polymorphisms are not useful as a genetic marker of tocilizumab efficacy in RA patients. More studies are necessary to confirm these results.
No conflict of interest.
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