系统性红斑狼疮分子病因研究进展

被引:18
作者
曹平
赵玉
王静
机构
[1] 兰州大学第二医院肾内科
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中图分类号
R593.241 [];
学科分类号
摘要
<正>系统性红斑狼疮(Systemic lupus erythematosus,SLE)是一种多系统损伤的自身免疫性疾病,以T、B细胞异常活化、补体激活、免疫复合物清除障碍、沉积、自身抗体的产生及免疫调节异常为特点[1,2]。世界流行病学调查为1.4%~21.9%,发病率为(7.4~159.4)/10万人,可造成多系统的损害,其中狼疮肾炎(Lupus nephritis,LN)是最严重的并发症之一,累积发病率亚洲人群最高,约为55%,非洲人群51%,其他各洲相对低,这些病人中23%约10年后发展为终末期肾病[3]。目前SLE病因、发病机理十分复杂,而且不同个体其发病机理不全相同[4]。
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页码:657 / 661+664 +664
页数:6
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