摘要
类风湿性关节炎(RA)是一种慢性自身免疫性疾病,可引起关节红肿、骨侵蚀进而导致畸形,通过NF-κB受体活化因子配体(RANKL)诱导破骨细胞分化是局部骨侵蚀和全身性骨质疏松发生发展的必要步骤。2010年6月美国食品和药物管理局批准Denosumab用于绝经后妇女骨质疏松症和前列腺癌患者激素抑制相关骨丢失的治疗。Denosumab作为RANKL特异性单抗,对RA患者骨关节侵蚀也具有很好的预防作用,本文基于核因子-κB受体活化因子/核因子-κB受体活化因子配体(RANK/RANKL)通路,从RA患者骨损伤机制与药物治疗现状出发,对Denosumab治疗RA患者骨损伤的临床研究进展作一综述。
Rheumatoid arthritis(RA)is a chronic autoimmune disease that can cause joint swelling,bone erosion and deformity.Induction of osteoclast differentiation through NF-κB receptor activator ligand(RANKL)is a necessary step for the occurrence and development of local bone erosion and systemic osteoporosis.In June 2010,FDA approved Denosumab for the treatment of hormone-inhibited bone loss in postmenopausal women with osteoporosis and prostate cancer.Denosumab,as a RANKL specific monoclonal antibody,also has a good protective effect on bone and joint erosion in RA patients.Based on the receptor activator of NF-κB/RANK ligand(RANK-RANKL)pathway,the mechanism of bone destruction in RA patients and the current status of drug treatment,this article reviews the clinical research progress of Denosumab in the treatment of bone destruction in RA patients.
作者
刘盈
周满如
黎卓熹
周春
LIU Ying;ZHOU Man-ru;LI Zhuo-xi;ZHOU Chun(School of Pharmacy,Xinhua College of Sun Yat-sen University,Guangzhou 510520,Guangdong Province,China;School of Pharmacy,Southern Medical University,Guangzhou 510515,Guangdong Province,China)
出处
《中国临床药理学杂志》
CAS
CSCD
北大核心
2021年第8期1012-1015,共4页
The Chinese Journal of Clinical Pharmacology
基金
广东省教育厅普通高校青年创新人才基金资助项目(2017KQNX257)。