Edwards N Lawrence
Department of Medicine, University of Florida, Gainesville, 32610-0221, USA.
Curr Opin Rheumatol. 2009 Mar;21(2):132-7. doi: 10.1097/BOR.0b013e3283257b96.
The role of uric acid as a mediator of vascular damage is not a new idea but has only recently gained widespread acceptance. Uric acid has previously been viewed as a benign solute in serum until it exceeds its saturation level. Others have viewed it as an important antioxidant. These opinions have given way to strong epidemiologic evidence that uric acid elevation may damage endothelial cells and cause significant medical problems.
The comorbidities associated with gout include hypertension, renal failure, obesity and diabetes. Multiple large epidemiologic studies cited in this review show that uric acid itself may play an important role in initiating the vascular endothelial dysfunction associated with this cluster of medical problems and ultimately lead to stroke, coronary artery disease and chronic kidney disease. These studies are supported by experiments in animals demonstrating how uric acid can gain entrance into cells and function as a 'pro-oxidant'.
Uric acid has been long recognized as the cause of gouty arthritis and kidney stones. There is mounting evidence that it may also have an important role in the development of vascular conditions such as coronary heart disease, stroke and kidney disease. These findings have important implications for the way we view asymptomatic hyperuricemia and for future therapeutic interventions.
尿酸作为血管损伤介质的作用并非新观点，但直到最近才得到广泛认可。尿酸此前一直被视为血清中的一种良性溶质，直到其超过饱和水平。其他人则将其视为一种重要的抗氧化剂。这些观点已让位于强有力的流行病学证据，即尿酸升高可能损害内皮细胞并引发严重的医学问题。
与痛风相关的合并症包括高血压、肾衰竭、肥胖症和糖尿病。本综述中引用的多项大型流行病学研究表明，尿酸本身可能在引发与这一系列医学问题相关的血管内皮功能障碍中起重要作用，并最终导致中风、冠状动脉疾病和慢性肾病。动物实验支持了这些研究，这些实验证明了尿酸如何进入细胞并作为“促氧化剂”发挥作用。
尿酸长期以来一直被认为是痛风性关节炎和肾结石的病因。越来越多的证据表明，它在诸如冠心病、中风和肾病等血管疾病的发展中可能也起着重要作用。这些发现对我们看待无症状高尿酸血症的方式以及未来的治疗干预具有重要意义。
