Aim: To assess the oxidative stress status in rheumatoid arthritis by measuring markers of free radical production, systemic activity of disease, free radical mediated tissue destruction and levels of antioxidant.
Methods:Peripheral blood samples were used for all the assays. Total nitric oxide (NO) was quantitatively measured using immunoassay kit. Malondialdehyde (MDA) and vitamin E were measured by spectrophotometric methods.Results: Statistically significant changes were observed in the levels of MDA, vitamin E, total NO and erythrocyte sedimentation rate (ESR) in the patient group. Significant differences were also observed in ESR and vitamin E levels in patients with active disease.
Conclusions:Increased oxidative stress status exists, which may lead to connective tissue degradation leading to joint and periarticular deformities in rheumatoid arthritis.
Tumor necrosis factor-alpha (TNF-α) is a proinflammatory cytokine that plays a pivotal role in regulating the inflammatory response in rheumatoid arthritis (RA). Although it is controversial whether TNF-α genes are associated with RA susceptibility, they are well known to mediate RA pathogenesis. We review in depth the history, formation and biological action, TNF receptor, role in mediating pathogenesis in RA and mode of action, of anti-TNF-α drugs.
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