Rheumatoid arthritis (RA) is a chronic autoimmune disorder marked by progressive joint inflammation that results in the destruction of cartilage and bone. With a global prevalence of 0.5-1%, the disease exhibits a significant female predominance, occurring at a 2-3:1 ratio compared to males. The pathogenesis of RA involves a complex interplay of genetic factors, particularly HLA-DRB1 alleles, environmental triggers such as smoking, and dysregulated immune responses. Diagnosis relies on a combination of clinical evaluation, serological testing for rheumatoid factor (RF) and anti-citrullinated peptide antibodies (ACPAs), and advanced imaging techniques including X-ray, ultrasound, and MRI. Contemporary management of RA follows a treat-to-target paradigm, with the primary goal of achieving remission or low disease activity. The therapeutic arsenal includes nonsteroidal anti-inflammatory drugs (NSAIDs) for symptomatic relief, corticosteroids as short-term bridge therapy, and disease-modifying antirheumatic drugs (DMARDs) as foundational treatment. DMARDs encompass conventional agents like methotrexate, targeted synthetic drugs such as JAK inhibitors, and biologic therapies including anti-TNF and anti-IL6 agents. First-line treatment typically begins with methotrexate, with escalation to combination therapies or biologics in cases of inadequate response. Regular monitoring every three months is essential to prevent irreversible joint damage and functional disability. Although RA remains incurable, advancements in treatment have substantially improved patient outcomes. Future directions in RA management emphasize personalized medicine strategies and the development of safer, more targeted therapies. Ongoing research continues to unravel the underlying mechanisms of RA, paving the way for novel and more effective treatment modalities.
Othman Othman (2025) studied this question.