Rheumatoid arthritis is an autoimmune disease of unknown etiology, characterized by articular inflammation. Oxidative damage induced by reactive oxygen species has been related to the pathophysiology of rheumatoid arthritis in several studies, although results have been inconsistent and contradictory.
To determine oxidative stress markers in patients with rheumatoid arthritis.
Descriptive cross-sectional study in rheumatoid arthritis patients and healthy controls. In peripheral blood samples from all study subjects, lipid peroxide (thiobarbituric acid reactive substances) and protein carbonyl levels were quantified as oxidative damage markers; superoxide dismutase and glutathione peroxidase activities, glutathione concentration, and the reduced glutathione/oxidized glutathione ratio were analyzed as antioxidant defense indicators. Mann-Whitney U tests were run. Statistical significance (a) was 0.05%.
We included 29 rheumatoid arthritis patients, 10 with active disease, and 41 healthy controls. Age was higher in the rheumatoid arthritis group; there were no differences in female:male ratio between groups. Oxidative damage was higher in rheumatoid arthritis patients; however, there was no difference between patients with active or inactive rheumatoid arthritis. Antioxidant enzyme activities, glutathione concentration, and reduced glutathione/oxidized glutathione ratio were higher in rheumatoid arthritis patients than in controls.
Antioxidant levels were higher in rheumatoid arthritis patients than in healthy controls; however, they were insufficient to prevent oxidative damage. This suggests an active oxidative process in rheumatoid arthritis patients.