Serum uric acid increases in patients with systemic autoimmune rheumatic diseases after 3 months of treatment with TNF inhibitors
Language English Country Germany Media print-electronic
Document type Journal Article
Grant support
No.940517
Grantová Agentura, Univerzita Karlova
00023728
Ministerstvo Zdravotnictví Ceské Republiky
19-18005Y
Grantová Agentura České Republiky
PubMed
31363829
DOI
10.1007/s00296-019-04394-6
PII: 10.1007/s00296-019-04394-6
Knihovny.cz E-resources
- Keywords
- Cytokines, Inflammation, Oxidative stress, Rheumatic diseases, Uric acid,
- MeSH
- Allantoin blood MeSH
- Antirheumatic Agents adverse effects MeSH
- Autoimmune Diseases blood diagnosis drug therapy immunology MeSH
- Biomarkers blood MeSH
- Time Factors MeSH
- Cytokines blood MeSH
- Adult MeSH
- Hyperuricemia blood chemically induced diagnosis MeSH
- Tumor Necrosis Factor Inhibitors adverse effects MeSH
- Uric Acid blood MeSH
- Middle Aged MeSH
- Humans MeSH
- Adolescent MeSH
- Young Adult MeSH
- Oxidative Stress MeSH
- Registries MeSH
- Rheumatic Diseases blood diagnosis drug therapy immunology MeSH
- Risk Factors MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Up-Regulation MeSH
- Treatment Outcome MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Adolescent MeSH
- Young Adult MeSH
- Male MeSH
- Aged, 80 and over MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Allantoin MeSH
- Antirheumatic Agents MeSH
- Biomarkers MeSH
- Cytokines MeSH
- Tumor Necrosis Factor Inhibitors MeSH
- Uric Acid MeSH
In patients with gout, the serum uric acid (SUA) is usually lower during acute gouty attacks than during intercritical periods. It has been suggested that systemic inflammatory response can cause this phenomenon. The objective is to determine whether therapy with TNF inhibitors (TNFis) affects SUA levels in patients with systemic autoimmune rheumatic diseases (SARDs) and whether SUA changes correlate with pro-inflammatory cytokines or with the oxidative stress marker allantoin. In this study, SUA, CRP, creatinine, 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, and allantoin levels were measured prior to and after 3 months of TNFis treatment in patients with SARDs. The values obtained in the biochemical assays were then tested for associations with the patients' demographic and disease-related data. A total of 128 patients (rheumatoid arthritis, n = 44; ankylosing spondylitis, n = 45; psoriatic arthritis, n = 23; and adults with juvenile idiopathic arthritis, n = 16) participated in this study. Among the entire patient population, SUA levels significantly increased 3 months after starting treatment with TNFis (279.5 [84.0] vs. 299.0 [102.0] μmol/l, p < 0.0001), while the levels of CRP, IL-6, IL-8, and MCP-1 significantly decreased. Male sex was the most powerful baseline predictor of ΔSUA in univariate and multivariate models. None of the measured laboratory-based parameters had statistically significant effects on the magnitude of ΔSUA. 3 months of anti-TNF therapy increased the levels of SUA in patients with SARDs, but neither the measured pro-inflammatory cytokines nor the oxidation to allantoin appeared responsible for this effect.
Department of Analytical Chemistry Faculty of Science Charles University Prague Czech Republic
Department of Rheumatology 1st Faculty of Medicine Charles University Prague Czech Republic
Institute of Rheumatology Na Slupi 4 128 50 Prague 2 Czech Republic
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