| Autor: |
Sunao Kojima, Kazuaki Uchiyama, Naoto Yokota, Eiichi Tokutake, Yutaka Wakasa, Shinya Hiramitsu, Masako Waki, Hideaki Jinnouchi, Hirokazu Kakuda, Takahiro Hayashi, Naoki Kawai, Masahiro Sugawara, Hisao Mori, Kenichi Tsujita, Kunihiko Matsui, Ichiro Hisatome, Yusuke Ohya, Kazuo Kimura, Yoshihiko Saito, Hisao Ogawa |
| Rok vydání: |
2022 |
| Předmět: |
|
| Zdroj: |
Cardiovascular drugs and therapyReferences. |
| ISSN: |
1573-7241 |
| Popis: |
Purpose: Inflammation plays an important role in the initiation and progression of atherosclerosis, leading to poor clinical outcomes. Hyperuricemia is associated with the activation of the Nod-like receptor protein 3 inflammasome. Here, we investigated whether inhibition of inflammation using febuxostat lowered the risk of cardiovascular events. Methods: This is a post-hoc analysis of the randomized trial, Febuxostat for Cerebral and CaRdiorenovascular Events PrEvEntion StuDy (FREED). In total, 1,067 patients (736 men and 331 women) were included in the analysis. We compared the serial changes in high-sensitivity C-reactive protein (hs-CRP) levels between febuxostat and non-febuxostat groups and assessed the correlation between the changes in uric acid (UA) and hs-CRP levels after febuxostat treatment. We also determined whether febuxostat could reduce a hard endpoint, defined as a composite of cardiovascular events and all-cause mortality. Results: Serum UA levels in the febuxostat group were significantly lower than those in the non-febuxostat group after randomization (p> 0.2 mg/dL or those administered 40 mg of febuxostat, the drug did not reduce hs-CRP levels or decrease the hard endpoint. Conclusion: Febuxostat reduced the UA levels but did not affect the CRP levels, and therefore may fail to decrease cardiovascular outcomes after treatment. Trial Registration: ClinicalTrial.gov (NCT01984749).https://clinicaltrials.gov/ct2/show/NCT01984749 |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
|
Full text from SpringerLink