Serum uric acid increases in patients with systemic autoimmune rheumatic diseases after 3 months of treatment with TNF inhibitors
Jazyk angličtina Země Německo Médium print-electronic
Typ dokumentu časopisecké články
Grantová podpora
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-zdroje
- Klíčová slova
- Cytokines, Inflammation, Oxidative stress, Rheumatic diseases, Uric acid,
- MeSH
- alantoin krev MeSH
- antirevmatika škodlivé účinky MeSH
- autoimunitní nemoci krev diagnóza farmakoterapie imunologie MeSH
- biologické markery krev MeSH
- časové faktory MeSH
- cytokiny krev MeSH
- dospělí MeSH
- hyperurikemie krev chemicky indukované diagnóza MeSH
- inhibitory TNF škodlivé účinky MeSH
- kyselina močová krev MeSH
- lidé středního věku MeSH
- lidé MeSH
- mladiství MeSH
- mladý dospělý MeSH
- oxidační stres MeSH
- registrace MeSH
- revmatické nemoci krev diagnóza farmakoterapie imunologie MeSH
- rizikové faktory MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- upregulace MeSH
- výsledek terapie MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mladiství MeSH
- mladý dospělý MeSH
- mužské pohlaví MeSH
- senioři nad 80 let MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- alantoin MeSH
- antirevmatika MeSH
- biologické markery MeSH
- cytokiny MeSH
- inhibitory TNF MeSH
- kyselina močová 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
Zobrazit více v PubMed
Free Radic Biol Med. 1999 May;26(9-10):1231-7 PubMed
J Rheumatol. 2000 Feb;27(2):554 PubMed
Eur J Clin Nutr. 2000 Jun;54(6):508-13 PubMed
Free Radic Biol Med. 2001 Dec 1;31(11):1313-22 PubMed
Pharmacol Res. 2002 May;45(5):361-8 PubMed
J Rheumatol. 2002 Sep;29(9):1950-3 PubMed
Am J Physiol. 1976 May;230(5):1276-83 PubMed
Cytogenet Cell Genet. 1992;61(2):121-2 PubMed
Nature. 2003 Oct 2;425(6957):516-21 PubMed
Annu Rev Immunol. 2005;23:787-819 PubMed
Clin Chim Acta. 2006 Mar;365(1-2):249-56 PubMed
Curr Pharm Des. 2005;11(32):4161-75 PubMed
Eur Heart J. 2006 May;27(10):1174-81 PubMed
Rheumatology (Oxford). 2007 Sep;46(9):1466-70 PubMed
J Hum Hypertens. 2008 Mar;22(3):177-82 PubMed
Immunol Rev. 2008 Jun;223:7-19 PubMed
Ann Rheum Dis. 2009 Oct;68(10):1602-8 PubMed
J Biol Chem. 1977 Oct 10;252(19):6721-8 PubMed
Arthritis Res Ther. 2010;12(2):206 PubMed
Chem Biol Interact. 1990;73(2-3):235-47 PubMed
PLoS One. 2011;6(5):e19901 PubMed
PLoS One. 2012;7(10):e46424 PubMed
Rheumatology (Oxford). 2013 Apr;52(4):676-8 PubMed
J Dermatolog Treat. 2014 Feb;25(1):83-6 PubMed
Rheum Dis Clin North Am. 2014 May;40(2):329-41 PubMed
Biomed Res Int. 2014;2014:675108 PubMed
Rheumatology (Oxford). 2014 Nov;53(11):1958-65 PubMed
Nat Rev Rheumatol. 2014 Dec;10(12):720-7 PubMed
Clin Exp Immunol. 2016 Jun;184(3):308-17 PubMed
Sci Rep. 2017 Jan 13;7:39884 PubMed
Oxid Med Cell Longev. 2017;2017:6501046 PubMed
Biochem J. 1987 May 1;243(3):803-8 PubMed
Arthritis Rheum. 1965 Oct;8(5):694-706 PubMed
Proc Natl Acad Sci U S A. 1981 Nov;78(11):6858-62 PubMed
Pediatr Res. 1995 Feb;37(2):219-26 PubMed
JAMA. 1994 Jan 26;271(4):302-3 PubMed
Free Radic Biol Med. 1993 Jun;14(6):615-31 PubMed
Ann Rheum Dis. 1997 Nov;56(11):696-7 PubMed
Ann Rheum Dis. 1998 Jul;57(7):443-4 PubMed
