雄激素剥夺治疗前列腺癌引起的骨代谢变化

ADT-associated osteoporosis in prostate cancer:adaptive response,mechanisms,and interactions with hormone

雄激素剥夺治疗(androgen deprivation therapy,ADT)是治疗转移性前列腺癌(PCa)的基石,显著延长了PCa患者生存期。然而在ADT治疗的PCa患者中,每年平均骨密度下降2%~10%,导致骨折发病率、相关发病率和死亡率增加,应该引起临床医师的注意。这种骨代谢状态,目前认为主要是雄激素、雌激素水平明显减低导致。临床工作者可通过监测骨转换指标、骨密度及FRAX算法筛选出需要提前干预的患者,并对该类患者提供生活方式的指导及干预,以达到减少骨质不良事件的发生。这些干预措施包括适当锻炼、减少吸烟喝酒、补充钙和维生素D、双膦酸盐、部分选择性雌激素受体调节剂(如托瑞米芬)和靶向RANK配体抑制剂等。

Androgen deprivation therapy(ADT)is the cornerstone of the treatment of metastatic prostate cancer(PCa).Although ADT could significantly improve the survival rate of PCa patients,the average annual bone mineral density of patients with PCa undergoing ADT decreases by 2%—10%,which leads to the increase of fracture incidence and related mortality.Clinicians should pay more attention to these metabolic changes.Notably,this state of bone metabolism is mainly caused by the reduction of androgen and estrogen.By clinical application of the bone metabolic markers,BMD and FRAX algorithm,clinicians can select patients who need early intervention,and provide lifestyle guidance and intervention for these patients,so as to reduce the occurrence of adverse events of bone.These interventions include appropriate exercise,reducing smoking and alcohol drinking,calcium and vitamin D supplementation,bisphosphonates,some selective estrogen receptor modulators(such as toremifene)and targeted RANK ligand inhibitors.