In Vivo Effects of Nonselective, Partially Selective, and Selective Non Steroidal Anti-Inflammatory Drugs on Lipid Peroxidation and Antioxidant Enzymes in Patients with Rheumatoid Arthritis: A Clinical Study

BACKGROUND: The relationship between oxidative stress, decreased antioxidant status, and rheumatoid arthritis (RA) has been widely investigated. To date, few clinical studies have assessed the role of conventional nonsteroidal anti-inflammatory drugs (NSAIDs) in the modulation of oxidative stress in patients with RA. AIM: The aim of this study was to compare the effects of nonselective, partially selective, and selective cyclooxygenase (COX) inhibitors on markers of oxidative stress in patients with RA. MATERIALS AND METHODS: Thirty RA patients were enrolled in this open label, prospective study for 12 weeks and randomly assigned to either group receiving diclofenac 100 mg, meloxicam 15 mg, or celecoxib 200 mg daily (n = 10 in each group). Patients were evaluated for superoxide dismutase (SOD) and serum malondialdehyde (MDA) as oxidative markers at the baseline and at the end of 12 weeks. Various parameters for efficacy were also assessed. RESULTS: The baseline values of the SOD enzyme were significantly lower and MDA values were significantly elevated in patients randomized to the three treatment groups as compared to the control group (P < 0.05). MDA level was significantly decreased in patients across all the treatment groups (P < 0.05) after 12 weeks. There was an improvement in mean SOD enzyme levels at the end of 12 weeks; the difference for SOD was significant as compared to the baseline in the meloxicam group only (P < 0.05) but not in diclofenac- and celecoxib-treated patients. Significant improvement was observed in all the treatment groups as regards patient assessment of pain visual analog scale, tender and swollen joint count, and patient global assessment. CONCLUSIONS: Diclofenac, meloxicam, and celecoxib carry antioxidant effects to a variable extent. NSAID possesses additional mechanism independent of COX inhibition which modulates oxidative stress.