高尿酸血症与内皮功能障碍  

Hyperuricemia and endothelial dysfunction

作　　者：刘华英[1] 顾丹阳[1] 邵加庆[1] 

机构地区：[1]南京军区南京总医院内分泌科,210002

出　　处：《国际内分泌代谢杂志》2016年第6期412-415,共4页International Journal of Endocrinology and Metabolism

摘　　要：高尿酸血症是常见的与代谢综合征相关的疾病，其与内皮细胞功能障碍的发生密切相关。尿酸既可以通过增强细胞内氧化应激、上调内皮细胞内的Ras-丝裂原活化蛋白激酶信号转导通路、引起线粒体钙离子显著超负荷和活性氧簇产生增加、降低一氧化氮和内皮型一氧化氮合酶（eNOS）的产生等直接损害血管内皮细胞的功能，又能够通过其常伴随的低脂联素血症、高瘦素血症和与高尿酸血症互为相关的胰岛素抵抗等共同影响磷脂酰肌醇3激酶-蛋白激酶B-eNOS和AMP活化蛋白激酶-eNOS等信号通路，间接损害内皮功能。虽然目前对于无症状高尿酸血症是否应该给予临床干预尚存在争议，但许多证据支持高尿酸血症可损害内皮功能，应当适当时机给无症状高尿酸血症患者予以干预。Hyperuricemia is a common disease that is related to metabolic syndrome and has relationship with the occurrence of endothelial dysfunction. Uric acid can induce endothelial dysfunction directly by increasing the oxidative stress, upregulating Ras-mitogen-activated protein kinase signal transduction pathway, inducing mitoehondrial calcium overload significantly, reducing the production and bio-utilization of nitric oxide. In addition, by the accompanied diseases of hyperurieemia such as insulin resistance, hypoa- diponectinaemia and hyperleptinemia, hyperuricemia can also cause endothelial dysfunction indirectly through affecting many pathways, such as the phosphatidyl inositol 3 kinase/serine-threonine protein kinase （Akt）/endothelial nitric oxide synthase and AMP activated protein kinase-endothelial nitric oxide synthase pathways. Whether to receive urate-lowering therapy or not hasn＇t reached a consensus for those patients with asymptomatic hyperuricemia. But after analyzing the relation between hyperuricemia and endothelial dysfunction, there are evidences supporting giving those asymptomatic hyperuricemic patients urate-lowering therapy at the right time.

关 键 词：高尿酸血症 内皮功能障碍 胰岛素抵抗 低脂联素血症 高瘦素血症 

分 类 号：R544.1[医药卫生—心血管疾病]