-
Je něco špatně v tomto záznamu ?
Serum uric acid increases in patients with systemic autoimmune rheumatic diseases after 3 months of treatment with TNF inhibitors
L. Hasikova, M. Pavlikova, H. Hulejova, P. Kozlik, K. Kalikova, A. Mahajan, M. Herrmann, B. Stiburkova, J. Zavada,
Jazyk angličtina Země Německo
Typ dokumentu časopisecké články
Grantová podpora
No.940517
Grantová Agentura, Univerzita Karlova
00023728
Ministerstvo Zdravotnictví Ceské Republiky
19-18005Y
Grantová Agentura České Republiky
NLK
ProQuest Central
od 1997-03-01 do Před 1 rokem
Medline Complete (EBSCOhost)
od 2000-12-01 do Před 1 rokem
Health & Medicine (ProQuest)
od 1997-03-01 do Před 1 rokem
- 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
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
Institute of Rheumatology Na Slupi 4 128 50 Prague 2 Czech Republic
Citace poskytuje Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc20006094
- 003
- CZ-PrNML
- 005
- 20210217114523.0
- 007
- ta
- 008
- 200511s2019 gw f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.1007/s00296-019-04394-6 $2 doi
- 035 __
- $a (PubMed)31363829
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a gw
- 100 1_
- $a Hasikova, Lenka $u Institute of Rheumatology, Na Slupi 4, 128 50, Prague 2, Czech Republic. Department of Rheumatology, First Faculty of Medicine, Charles University, Prague, Czech Republic.
- 245 10
- $a Serum uric acid increases in patients with systemic autoimmune rheumatic diseases after 3 months of treatment with TNF inhibitors / $c L. Hasikova, M. Pavlikova, H. Hulejova, P. Kozlik, K. Kalikova, A. Mahajan, M. Herrmann, B. Stiburkova, J. Zavada,
- 520 9_
- $a 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.
- 650 _2
- $a mladiství $7 D000293
- 650 _2
- $a dospělí $7 D000328
- 650 _2
- $a senioři $7 D000368
- 650 _2
- $a senioři nad 80 let $7 D000369
- 650 _2
- $a alantoin $x krev $7 D000481
- 650 _2
- $a antirevmatika $x škodlivé účinky $7 D018501
- 650 _2
- $a autoimunitní nemoci $x krev $x diagnóza $x farmakoterapie $x imunologie $7 D001327
- 650 _2
- $a biologické markery $x krev $7 D015415
- 650 _2
- $a cytokiny $x krev $7 D016207
- 650 _2
- $a ženské pohlaví $7 D005260
- 650 _2
- $a lidé $7 D006801
- 650 _2
- $a hyperurikemie $x krev $x chemicky indukované $x diagnóza $7 D033461
- 650 _2
- $a mužské pohlaví $7 D008297
- 650 _2
- $a lidé středního věku $7 D008875
- 650 _2
- $a oxidační stres $7 D018384
- 650 _2
- $a registrace $7 D012042
- 650 _2
- $a revmatické nemoci $x krev $x diagnóza $x farmakoterapie $x imunologie $7 D012216
- 650 _2
- $a rizikové faktory $7 D012307
- 650 _2
- $a časové faktory $7 D013997
- 650 _2
- $a výsledek terapie $7 D016896
- 650 _2
- $a inhibitory TNF $x škodlivé účinky $7 D000079424
- 650 _2
- $a upregulace $7 D015854
- 650 _2
- $a kyselina močová $x krev $7 D014527
- 650 _2
- $a mladý dospělý $7 D055815
- 655 _2
- $a časopisecké články $7 D016428
- 700 1_
- $a Pavlikova, Marketa $u Department of Probability and Mathematical Statistics, Faculty of Mathematics and Physics, Charles University, Prague, Czech Republic.
- 700 1_
- $a Hulejova, Hana $u Institute of Rheumatology, Na Slupi 4, 128 50, Prague 2, Czech Republic.
- 700 1_
- $a Kozlík, Petr $u Department of Analytical Chemistry, Faculty of Science, Charles University, Prague, Czech Republic. $7 xx0257220
- 700 1_
- $a Kalikova, Kveta $u Department of Physical and Macromolecular Chemistry, Faculty of Science, Charles University, Prague, Czech Republic.
- 700 1_
- $a Mahajan, Aparna $u Department of Internal Medicine 3, Rheumatology and Immunology, Friedrich-Alexander University of Erlangen-Nürnberg, Erlangen, Germany.
- 700 1_
- $a Herrmann, Martin $u Department of Internal Medicine 3, Rheumatology and Immunology, Friedrich-Alexander University of Erlangen-Nürnberg, Erlangen, Germany.
- 700 1_
- $a Stiburkova, Blanka $u Institute of Rheumatology, Na Slupi 4, 128 50, Prague 2, Czech Republic. Department of Pediatrics and Adolescent Medicine, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czech Republic.
- 700 1_
- $a Zavada, Jakub $u Institute of Rheumatology, Na Slupi 4, 128 50, Prague 2, Czech Republic. zavada@revma.cz. Department of Rheumatology, First Faculty of Medicine, Charles University, Prague, Czech Republic. zavada@revma.cz.
- 773 0_
- $w MED00004228 $t Rheumatology international $x 1437-160X $g Roč. 39, č. 10 (2019), s. 1749-1757
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/31363829 $y Pubmed
- 910 __
- $a ABA008 $b sig $c sign $y a $z 0
- 990 __
- $a 20200511 $b ABA008
- 991 __
- $a 20210217114438 $b ABA008
- 999 __
- $a ok $b bmc $g 1524952 $s 1096150
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2019 $b 39 $c 10 $d 1749-1757 $e 20190731 $i 1437-160X $m Rheumatology international $n Rheumatol Int $x MED00004228
- GRA __
- $a No.940517 $p Grantová Agentura, Univerzita Karlova
- GRA __
- $a 00023728 $p Ministerstvo Zdravotnictví Ceské Republiky
- GRA __
- $a 19-18005Y $p Grantová Agentura České Republiky
- LZP __
- $a Pubmed-20200511
