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Serum uric acid increases in patients with systemic autoimmune rheumatic diseases after 3 months of treatment with TNF inhibitors

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11310%2F19%3A10400640" target="_blank" >RIV/00216208:11310/19:10400640 - isvavai.cz</a>

  • Alternative codes found

    RIV/00216208:11110/19:10400640 RIV/00023728:_____/19:N0000068

  • Result on the web

    <a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=dSJZOXlHg5" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=dSJZOXlHg5</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1007/s00296-019-04394-6" target="_blank" >10.1007/s00296-019-04394-6</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Serum uric acid increases in patients with systemic autoimmune rheumatic diseases after 3 months of treatment with TNF inhibitors

  • Original language description

    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-alpha 2, IFN-gamma, Il-1 beta, IL-6, IL-8, IL-10, IL-12, IL-17a, IL-18, IL-23, IL-33, TNF-alpha, 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&apos; 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] mu mol/l, p &lt; 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 Delta SUA in univariate and multivariate models. None of the measured laboratory-based parameters had statistically significant effects on the magnitude of Delta SUA. 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.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    30226 - Rheumatology

Result continuities

  • Project

    <a href="/en/project/GJ19-18005Y" target="_blank" >GJ19-18005Y: Retention mechanisms of intact glycopeptides in hydrophilic interaction liquid chromatography</a><br>

  • Continuities

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Others

  • Publication year

    2019

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Rheumatology International

  • ISSN

    0172-8172

  • e-ISSN

  • Volume of the periodical

    39

  • Issue of the periodical within the volume

    10

  • Country of publishing house

    DE - GERMANY

  • Number of pages

    9

  • Pages from-to

    1749-1757

  • UT code for WoS article

    000485314900010

  • EID of the result in the Scopus database

    2-s2.0-85069947650