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Objective: Hyperuricemia is a common disease related to metabolic syndrome. Since only 10% of hyperuricemic patients will develop gout, there is a lack of consensus in regards to whether patients with asymptomatic hyperuricemia should receive uric acid lowering treatment. This article discusses the endothelial dysfunction induced by hyperuricemia and summarizes published evidence on the treatment of asymptomatic hyperuricemia.
Findings: Hyperuricemia is related to chronic kidney disease (CKD), cardiovascular disease (CVD), hypertension, and insulin resistance, which are relevant to the mortality rate seen in hyperuricemia. With increased obesity and CKD and changes to dietary structure and lifestyle, the prevalence of hyperuricemia is increasing. Uric acid can induce endothelial dysfunction per se by increasing oxidative stress and inflammatory response and reducing the production and bio-utilization of nitric oxide (NO). Hyperuricemia is suggested to be a simple and important marker of insulin resistance and is negatively related to serum adiponectin level and positively related to leptin level. The accompanied diseases of hyperuricemia including insulin resistance, hypoadiponectinaemia and hyperleptinemia can also cause endothelial dysfunction through affecting many pathways.
Conclusion: Many researchers support giving asymptomatic hyperuricemic patients uric acid lowering treatment in time to prevent endothelial dysfunction, but there is no consensus on optimal uric acid treatment levels. Further interventional studies are required.