骨癌痛发病机制及临床治疗进展  

Cance-induced Bone Pain： Mechanism and Clinical Treatment Progress

作　　者：徐嘉莹[1] 刘薇[1] 黄宇光[1] 

机构地区：[1]中国科学医学院北京协和医院麻醉科,北京100073

出　　处：《麻醉与监护论坛》2010年第4期297-299,共3页Forum of Anesthesia and Monitoring

摘　　要：转移性癌性骨痛（metastatic cancer—induced bonepain、CIBP）的发病率较高，然而由于其发病机制复杂、研究不清使得传统镇痛疗法效果不佳。现有研究结论提示．该病的发病机制分为外周因素和中枢因素．肿瘤骨微环境中破骨细胞的持续活化、免疫细胞和炎症因子激活导致的疼痛敏化、肿瘤组织对骨膜的直接压迫浸润、以及脊髓神经生化改变等因素均影响CIBP的发生。目前常用的镇痛方法仍为多药联合治疗。药物包括阿片类药物．非甾体类抗炎药、双膦酸盐、谷氨酸抑制剂和NMDA拮抗剂等。Metastatic cancer-induced bone pain（CIBP） has a very high incidence rate but poor analgesic response due to its complicated and unclear mechanism. The current studies indicate that CIBP has both peripheral and central mechanism, including constant osteoclastogenesis and acitivation of inflammatory factors in the tumor bone micro-environment, direct compression of tumor tissue to the periesteum, neurochemical changes in the spinal cord etc.Multi-module treatment is widely used, containing opioids, NSAIDs, bisphosphonates, glutamate inhibitor and NMDA antagonist.

关 键 词：转移性癌性骨痛 发病机制 破骨细胞活化 交叉对话 

分 类 号：R657.4[医药卫生—外科学]