尿酸、高尿酸血症与缺血性卒中

Uric acid, hyperuricemia and ischemic stroke

尿酸是嘌呤代谢的终产物.高尿酸血症定义为血尿酸＞ 420 μmol/L（男性）和360μmol/L（女性）.多种机制可引起血尿酸水平增高.系统评价和汇总分析显示,高尿酸血症与缺血性卒中患者发病率和病死率增高均显著相关.然而,尿酸作为一种强效抗氧化剂和自由基清除剂,似乎在缺血性卒中中具有神经保护作用.早期给予尿酸可增强血栓栓塞性卒中大鼠重组组织型纤溶酶原激活剂（recombinant tissue plasminogen activator,rtPA）溶栓治疗的效果.因此,有必要对rtPA溶栓与尿酸联合应用在急性缺血性卒中患者中的临床效果进行随机对照试验.一项3期临床试验正在进行中,其结果值得期待.

Uric acid is an end product of purine metabolism. Hyperuricemia is defined as serum uric acid level 〉420 μmol/L in man, and 360 μmol/L in woman. Several mechanisms can cause elevated serum uric acid levels. Systematic reviews and Meta-analyses have shown that hyperuricemia is significantly correlated with the increased morbidity and mortality in patients with ischemic stroke. However, as a powerful antioxidant and a radical scavenger, uric acid seems to have a neuroprotective effect in ischemic stroke. Uric acid administered early can enhance the effect of recombinant tissue plasminogen activator （rtPA） thrombolytic therapy in rats with thromboembolic stroke. Therefore, it is necessary to conduct a randomized controlled trial for the clinical effects of rtPA thrombolysis in combination with uric acid in patients with acute ischemic stroke. A phase 3 clinical trial is ongoing, and its results are worth waiting for.