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痛风发病机制研究进展 被引量：19

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摘要 痛风是长期嘌呤代谢障碍及(或)尿酸排泄减少,血尿酸增高引起组织损伤的一组临床综合征。人类由于缺乏尿酸酶不能将嘌呤代谢产生的尿酸分解为可溶性的尿囊素排出体外,使尿酸成为人类嘌呤代谢的终产物。而与嘌呤代谢有关的酶活性的改变、与编码转运尿酸相关蛋白基因的突变以及尿酸盐结晶诱导的炎症反应,导致了痛风的形成及与痛风相关的各种症状的出现,从而使人们已开始从基因、分子水平来研究、认识此病。
作者 张瑞芬 赵晶
机构地区 中国人民解放军成都军区昆明总医院临床实验科
出处 《实用药物与临床》 CAS 2007年第4期244-246,共3页 Practical Pharmacy and Clinical Remedies
关键词 痛风 高尿酸血症 基因 分子基础 尿酸转运
分类号 R589.7 [医药卫生—内分泌]
  • 相关文献

参考文献26

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二级参考文献9

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实用药物与临床
2007年 第4期

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