The First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahata-nishi, Kitakyushu 807-8555, Japan.
Clinical Development Department, R&D Division, Daiichi Sankyo Co., Ltd., 1-2-58 Hiromachi, Shinagawa-ku, Tokyo 140-8710, Japan.
Curr Opin Pharmacol. 2018 Jun;40:110-119. doi: 10.1016/j.coph.2018.03.006. Epub 2018 Apr 24.
Rheumatoid arthritis (RA), a chronic inflammatory disorder, causes swelling, bone erosion, and joint deformity. Bone erosion in RA-affected joints arises from activation of osteoclasts by inflammatory processes. RA patients may also have primary, disease-related, or glucocorticoid-induced osteoporosis, caused by a disrupted balance between osteoclasts and osteoblasts. Disease-modifying antirheumatic drugs (DMARDs) interfere with the processes causing inflammation in the joint but do not sufficiently treat bone erosion and osteoporosis. Denosumab, an inhibitor of receptor activator of nuclear factor κ-B ligand (RANKL), protects bones in osteoporosis patients. Clinical studies have demonstrated that denosumab can also prevent bone erosion in RA patients. Because joint destruction progresses in some patients treated with DMARDs alone, denosumab will likely become standard treatment for some RA patients.
类风湿关节炎（RA）是一种慢性炎症性疾病，可导致肿胀、骨侵蚀和关节畸形。RA 关节中的骨侵蚀是由炎症过程激活破骨细胞引起的。RA 患者也可能患有原发性、与疾病相关或糖皮质激素诱导的骨质疏松症，这是由破骨细胞和成骨细胞之间的平衡被打破引起的。改变病情抗风湿药物（DMARDs）会干扰关节炎症的发生过程，但不能充分治疗骨侵蚀和骨质疏松症。地舒单抗是核因子κ-B 配体（RANKL）受体激活剂的抑制剂，可保护骨质疏松症患者的骨骼。临床研究表明，地舒单抗还可以预防 RA 患者的骨侵蚀。由于单独使用 DMARDs 治疗的某些患者关节破坏会进展，因此地舒单抗可能成为某些 RA 患者的标准治疗方法。
