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-a2, IFN-g, Il-1b, IL-6, IL-8, IL-10, IL-12, IL17a, IL-18, IL-23, IL-33, TNF-a). 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. 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).