急性痛风发作自发缓解的“关闭”机制。

The "switch-off" mechanism of spontaneous resolution of acute gout attack.

作者信息

Marcolongo R, Calabria A A, Lalumera M, Gerli R, Alessandrini C, Cavallo G

机构信息

Institute of Rheumatology, University of Siena, Italy.

出版信息

J Rheumatol. 1988 Jan;15(1):101-9.

PMID:2832599

Abstract

Urate crystal size change and the modification of coated proteins by oxygen radicals released by stimulated polymorphonuclear cells (PMN) could represent a likely "switch-off" mechanism of the spontaneous resolution of acute gout attack. The absorption spectra and the uric acid, allantoin and urea concentrations were determined before and after in vitro exposition of monosodium urate (MSU) crystals to superoxide anion (O2) photochemically generated. The results showed a complete dissolution of MSU crystals after incubation under O2-, with decrease of uric acid and increase of allantoin and urea concentrations. Our results were confirmed by polarizing, electron microscopy and calorimetric techniques. The results obtained seem to confirm that the spontaneous resolution of acute gout attack could be attributed to the dissolving effect on urate crystals and the modification of coated proteins by O2- released by phagocytizing PMN.

摘要

尿酸盐晶体大小的变化以及受刺激的多形核细胞（PMN）释放的氧自由基对包被蛋白的修饰，可能代表了急性痛风发作自发缓解的一种可能的“关闭”机制。在尿酸钠（MSU）晶体体外暴露于光化学产生的超氧阴离子（O2）之前和之后，测定其吸收光谱以及尿酸、尿囊素和尿素的浓度。结果显示，在O2-环境下孵育后，MSU晶体完全溶解，尿酸浓度降低，尿囊素和尿素浓度升高。我们的结果通过偏振、电子显微镜和量热技术得到了证实。所获得的结果似乎证实，急性痛风发作的自发缓解可能归因于对尿酸盐晶体的溶解作用以及吞噬PMN释放的O2-对包被蛋白的修饰。