Background The dependence of intensity of carbonyl stress and its correlation with the pathogenic inflammatory and erosive process of joint tissue were determined in adults with rheumatoid arthritis. These issues in patients with juvenile idiopathic arthritis (JIA) were not studied.
Objectives It was to determine the role of content in the blood of carbonylated proteins (CP), the intensity of induced lipid peroxidation (LPO), the activity of superoxidedismutase (SOD), glutathioneperoxidase (GPO) and the correlations between them and the early immunological markers of the disease, such as anti-cyclic citrullinated peptide antibodies (a-CCP) and modified citrullinated vimentin antibody (a-MCV), at different stages of the disease development in patients with JIA.
Methods The study included 29 patients with oligoarticular and polyarticular forms of JIA within 2 – 18 years old. 12 healthy children of identical age and gender with the studying patients were present in the control group. For the statistic processing of the material Stagraphics 3.0 was used.
Results Investigated group included 21 female and 8 - male. Patients under 10 years predominated. In children with JIA increase of the intensity of induced LPO in comparison with persons of control group was presented (p<0.001) and did not depend on the duration of JIA, number of affected joints and inflammatory activity. Patients with oligoarthritis had higher values of induced LPO than with polyarthritis (p<0.05). The level of CB had a significant decrease in patients with JIA in comparison with persons of control group (p<0.05). It is presented in the first 6 months of the onset of the disease, mostly by patients with III degree of inflammatory activity. Variations of GPO activity in patients and the children of control group were not different, and did not depend on the form of arthritis, duration of disease, inflammatory activity. Rate of activity of SOD was lower in children with JIA in comparison with persons of control group (p<0.05). Among patients with positive a-CCP in comparison with children with positive a-MCV decrease of SOD activity was determined (p<0.05). A similar pattern was typical for JIA in the first 6 months of illness, during 6–12 months of pathological process development it was marked increase in SOD activity (p<0.05), and the longer history of the disease level of SOD activity was not different in comparison with control group. Level of SOD activity was authentically lower among patients with polyarthritis and with high degree of activity (p<0.05).
Conclusions Increasing of level of induced LPO was presented at early stage of JIA, with increasing duration of the disease it was also increased. For the first 6 months of JRA development level of CB in serum was decreased, especially in patients with high (III) degree of disease activity. Decreasing of SOD activity was determined in the first year of the disease's development, mainly in patients with polyarthritis, with II-III degree of inflammatory activity and positive titers of a-CCP. Activity of GPO was not different between patients and persons of control group. Reasonability and methods of correction of above-noted changes of parameters of antioxidant defense and lipid peroxidation in patients with juvenile idiopathic arthritis should be investigated further.
Disclosure of Interest None declared