ASSOCIATION OF NEUROLOGICAL COMPLICATIONS WITH HYPERHOMOCYSTEINEMIA IN CHILDREN WITH JUVENILE RHEUMATOID ARTHRITIS

Abstract

The pathogenesis of juvenile rheumatoid arthritis (JRA) is a complex process in which genetic, immune, and environmental factors interact. One aspect that has attracted research attention is the role of homocysteine, an amino acid resulting from the metabolism of methionine. One of the key mechanisms through which homocysteine may contribute to the development of SUR is its influence on inflammatory processes. Elevated levels of homocysteine can activate macrophages and other cells of the immune system, leading to the release of proinflammatory cytokines (e.g., interleukins and tumor necrosis factor). These molecules play a central role in the pathogenesis of inflammatory diseases, including arthritis. It is hypothesized that elevated homocysteine levels may contribute to the development of autoimmune reactions. This may occur through activation of T-lymphocytes and formation of antibodies against the body's own tissues. In the case of JRA, this can cause the immune system to attack the body's own joints, causing them to become inflamed and damaged. Homocysteine also plays a role in the pathogenesis of vascular disease. It can cause endothelial dysfunction and promote blood clot formation. These changes may affect the blood supply to joints, which exacerbates inflammatory processes and promotes arthritic changes.