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痛风与晶体诱导炎症的机制

Gout and mechanisms of crystal-induced inflammation.

作者信息

Terkeltaub R A

机构信息

Rheumatology Section, San Diego Veterans Affairs Medical Center, CA 92161.

出版信息

Curr Opin Rheumatol. 1993 Jul;5(4):510-6. doi: 10.1097/00002281-199305040-00017.

Abstract

Since last year's review of gout and hyperuricemia, investigators have described new potential mechanisms that may contribute to urate crystal deposition and the propagation, self-limitation, and therapeutic control of gouty inflammation. The clinical presentation of gout in women continues to be described in greater detail. Also, new information on oral allopurinol desensitization is now available to help approach the difficult problem of allopurinol hypersensitivity.

摘要

自去年对痛风和高尿酸血症进行综述以来,研究人员已经描述了一些新的潜在机制,这些机制可能导致尿酸盐晶体沉积以及痛风性炎症的传播、自我限制和治疗控制。女性痛风的临床表现仍在得到更详细的描述。此外,现在有关于口服别嘌醇脱敏的新信息,可帮助解决别嘌醇超敏反应这一难题。

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