2004
DOI: 10.1016/s0306-9877(03)00324-4
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Uric acid administration for neuroprotection in patients with acute brain ischemia

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Cited by 44 publications
(28 citation statements)
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“…19 However, the definitive proof of causality between increased UA levels and better stroke outcome requires an appropriately designed therapeutic controlled trial. 24 For this reason, the Spanish Drugs Agency has recently approved a multicenter clinical trial of UA administration in patients with acute stroke treated with alteplase and which is due to start in 2010 (EudraCT 2007-002687-95 and NCT00860366). …”
Section: Discussionmentioning
confidence: 99%
“…19 However, the definitive proof of causality between increased UA levels and better stroke outcome requires an appropriately designed therapeutic controlled trial. 24 For this reason, the Spanish Drugs Agency has recently approved a multicenter clinical trial of UA administration in patients with acute stroke treated with alteplase and which is due to start in 2010 (EudraCT 2007-002687-95 and NCT00860366). …”
Section: Discussionmentioning
confidence: 99%
“…Although adenine nucleotide concentrations and energy charge were not modified in our study, uric acid levels were increased in the IPC group. Although uric acid, a metabolite of the adenine nucleotide pathway, was previously thought to have a negative effect on I/R injury, it has recently been shown to have a beneficial effect as a very active scavenger (36,37). The high uric acid levels in the IPC group in our study suggest a better cell environment to eliminate toxic substances such as hypoxanthine and xanthine during reperfusion.…”
Section: Discussionmentioning
confidence: 99%
“…Interestingly, while other studies failed to confirm the independent, negative prospective relationship between UA and cardiovascular morbidity and mortality (Forman et al 2007;Coutinho et al 2007;Hozawa et al 2006;Wheeler et al 2005;Hu et al 2001;Moriarity et al 2000;Culleton et al 1999), evidence that UA is a protective factor or a marker of good health status is limited to few studies on acute cerebral ischemia (Chamorro et al 2004) and the protective effect of UA on oxidative stress generated during physical activity (Waring et al 2003). Several mechanisms may explain the hypothetical negative effect of uric acid on health, including a direct stimulating effect of soluble non-crystalline UA on inflammation, the impairment of endothelial function and the development of pro-oxidant properties in specific metabolic conditions (Maxwell and Bruinsma 2001;Alderman 2002;Hediger et al 2005).…”
Section: Introductionmentioning
confidence: 99%