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Abstract

The present study aimed to examine the role of Interleukin-6 (IL-6) promoter polymorphisms in the response to Etanercept (ETN) treatment in a group (Cohort) of Iraqi RA patients. Ninety active RA patients were chosen and studied at baseline, three to six months post-ETN therapy. The experiment was carried out in the Rheumatology unit at Baghdad Teaching Hospital in Medical City, Baghdad/Iraq. Based on the Disease Activity Score 28-Erythrocyte Sedimentation Rate (DAS28-ESR), the patients were categorized into responders and non-responders. The Results revealed that at baseline, responders were significantly younger than non-responders (P=0.0025). For the responders group; there were a significant enhancement in DAS28-ESR components (P<0.001), in all disease activity parameters included Patient and Provider Global Assessment (PtGA) and (PrGA), Tender Joint Count (TJC), Swollen Joint Count (SJC), Clinical Disease Activity Index (CDAI), DAS28-ESR post treatment, while low or negative reduction recorded for non-responders. In addition, the genetic tests disclosed a significant correlation between IL-6 rs1800795 genotypes and treatment response; the C allele of non-responders was more prominent (28.9% vs. 12.5%, P=0.0059), and GG carriers achieved a significantly greater reduction in DAS28-ESR after six months compared to GC and CC carriers (P<0.05). No significant linkage was detected for the rs1800796 or rs1800797 polymorphisms. In summary, the IL-6 rs1800795 C allele is associated with increased disease activity and nonresponsiveness to ETN in Iraqi RA patients, whereas the G allele predicts a favorable response. This polymorphism represents a potential biomarker for personalizing anti-TNF therapy‎.

Keywords: Polymorphism, IL-6, Etanercept, Anti-TNF, Rheumatoid arthritis

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