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高尿酸血症的发病机制:最新进展

Pathogenesis of hyperuricemia: recent advances.

作者信息

Ghei Manisha, Mihailescu Mihaela, Levinson Dennis

机构信息

Michael Reese Hospital, Department of Internal Medicine, 2929 South Ellis Avenue, Chicago, IL 60616, USA.

出版信息

Curr Rheumatol Rep. 2002 Jun;4(3):270-4. doi: 10.1007/s11926-002-0076-z.

Abstract

The literature on the pathogenesis of hyperuricemia have been limited to the discussion of metabolic syndromes associated with risk factors for atherosclerosis and hyperuricemia and the genetics of the juvenile form of hyperuricemic nephropathies. A few new mutations in the hypoxanthine-guanine phosphoribosyltransferase gene, which result in Lesch-Nyhan syndrome, have been described. In addition, some new insight has been gained in the renal handling of uric acid by the human kidney.

摘要

关于高尿酸血症发病机制的文献,一直局限于对与动脉粥样硬化和高尿酸血症风险因素相关的代谢综合征以及青少年型高尿酸血症肾病遗传学的讨论。已经描述了次黄嘌呤 - 鸟嘌呤磷酸核糖转移酶基因中的一些新突变,这些突变会导致莱施 - 奈恩综合征。此外,在人类肾脏对尿酸的处理方面也有了一些新的认识。

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