ASSOCIATION OF TNF-α GENE POLYMORPHISM WITH THE RISK AND SEVERITY OF RHEUMATOID ARTHRITIS

Abstract

Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by persistent synovial inflammation, which leads to progressive joint destruction and significant disability if not adequately treated [7]. Affecting up to 1% of the global population, RA presents a major public health challenge, severely impacting patients' quality of life and functional capacity [6]. The etiology of RA remains incompletely understood, but it is established as a multifactorial disease arising from a complex interplay between genetic predisposition and environmental factors [3, 7]. Among the numerous genetic factors under investigation, polymorphisms in the gene for tumor necrosis factor-alpha (TNF-α) have garnered considerable attention. TNF-α is a pivotal pro-inflammatory cytokine central to the pathogenesis of RA, and genetic variations, such as the TNF-α-308G/A polymorphism (rs1800629), may influence its production, thereby potentially affecting disease susceptibility and severity [3]. However, individual studies have yielded conflicting results regarding this association, with some reporting a significant link and others finding none [2, 4]. This inconsistency has necessitated large-scale systematic reviews and meta-analyses, conducted according to rigorous guidelines like PRISMA, to clarify the role of this polymorphism [5, 8].