exploring epidemiological, clinical, and autoimmune reactivity perspectives of rheumatoid arthritis after covid-19

Background: emerging evidence suggests that sars-cov-2 infection may contribute to the development or exacerbation of autoimmune diseases, including rheumatoid arthritis (ra), through mechanisms such as immune system hyperactivation, cytokine storm, and the production of autoantibodies.materials and methods: this review aimed to investigate the potential association between sars-cov-2 infection or vaccination and the onset or flare-up of ra, with a focus on pathogenic mechanisms, clinical features, diagnostic approaches, and therapeutic strategies. a collection of published case reports and studies was reviewed to identify patterns and clinical outcomes related to ra after covid-19 infection or vaccination.results: new-onset ra symptoms are most frequently observed within 2 to 16 weeks post-infection, with a higher incidence in women. common laboratory findings included elevated c-reactive protein (crp) and erythrocyte sedimentation rate (esr) levels, along with positive rheumatoid factor (rf) and anti-citrullinated protein antibodies (acpas). in some cases, a genetic predisposition was also identified, suggesting an interaction between genetic and environmental factors. despite the viral context, diagnosis and treatment strategies are largely aligned with standard ra protocols. ra onset or exacerbation following covid-19 vaccination appears to be rare, and the benefits of vaccination continue to outweigh the associated risks.conclusion: although current evidence suggests a potential association between sars-cov-2 infection and the pathogenesis of ra, existing studies are limited in scope and sample size. further large-scale, longitudinal research is required to substantiate these findings and better understand the underlying mechanisms.