AB0872 OXIDATIVE STRESS MARKER ALLANTOIN IS NOT ASSOCIATED WITH THE CHANGE OF SERUM URIC ACID LEVEL IN PATIENTS WITH SYSTEMIC RHEUMATIC DISEASES AFTER ABROGATION OF SYSTEMIC INFLAMMATION BY TNF INHIBITION

Abstract

Background In patients with gout, the serum uric acid (SUA) is usually lower during acute gouty attacks than during intercritical periods. In a previous study, we have shown that abrogation of systemic inflammation by TNF inhibitors (TNFi) results in an increase in the levels of SUA in patients with systemic rheumatic diseases. We have not found any correlation between the magnitude of change of SUA and CRP or pro-inflammatory cytokines (MCP-1, IFN-α2, IFN-γ, Il-1β, IL-6, IL-8, IL-10, IL-12, IL-17a, IL-18, IL-23, IL-33, TNF-α).1 Another possible mechanism for the lowering of SUA during inflammation may be consumption of circulating SUA in free radical reactions generated during systemic inflammation. Allantoin has been validated as a stable biomarker of oxidative stress in humans.2 Objectives We aimed to investigate whether the magnitude of change of SUA after starting therapy with TNFi is associated with the change of oxidative stress marker – allantoin in patients with systemic autoimmune rheumatic diseases: rheumatoid arthritis (RA), ankylosing spondylitis (AS), psoriatic arthritis (PsA) and juvenile idiopathic arthritis (JIA). Methods A cohort of 94 patients with clinically active chronic inflammatory rheumatic diseases (31 with RA, 33 with AS, 18 with PsA, 12 with JIA) and CRP > 10 mg/L was recruited in the Institute of Rheumatology, Prague. SUA, CRP and allantoin were measured before and after 3 months of treatment with TNFi. Assessment of allantoin in plasma samples was carried out on the Agilent Infinity 1290 system coupled with a Triple Quad 6460 tandem mass spectrometer. For the statistical analysis the ratio between the values at the baseline and values after 3 months of therapy with TNFi were used. We retrieved demographic data and disease characteristics. Results The levels of SUA have significantly increased after 3 months of treatment with TNFi (270.5 [78.8] vs. 303.0 [101.5] μmol/l, p Conclusion The abrogation of systemic inflammation by TNFi results in an increase in the levels of SUA in patients with systemic rheumatic diseases, but the mechanism remains elusive. We have not observed any correlation between the magnitude of change of SUA and CRP or oxidative stress marker allantoin.