Israeli Ron S, Ryan Christopher W, Jung Laura L
Staten Island Urological Research, Staten Island, New York, USA.
J Urol. 2008 Feb;179(2):414-23. doi: 10.1016/j.juro.2007.09.028.
We reviewed the pathogenesis, diagnosis, prevalence, prevention and treatment of bone loss in patients with nonmetastatic prostate cancer receiving androgen deprivation therapy.
Using PubMed we performed a comprehensive literature search to identify articles on bone mineral density loss in patients with nonmetastatic prostate cancer receiving androgen deprivation therapy. Pertinent articles were reviewed and evaluated.
Bone mineral density loss and related fractures were recently established as significant adverse events associated with androgen deprivation therapy. Patients with nonmetastatic prostate cancer receiving androgen deprivation therapy experience annual bone mineral density losses of 0.6% to 4.6% with the most significant loss within year 1 of therapy. In addition to calcium and vitamin D supplements, current treatment options for androgen deprivation therapy induced bone loss include synthetic estrogens, selective estrogen receptor modulators and bisphosphonates. Recent safety concerns have been identified, including renal dysfunction with intravenous bisphosphonates and osteonecrosis of the jaw with oral and intravenous bisphosphonates. However, minimal renal dysfunction and no cases of osteonecrosis of the jaw have been reported in this setting.
Because the most significant bone mineral density loss occurs within year 1 of androgen deprivation therapy and most fractures in healthy men occur in those without osteoporosis, early intervention is warranted to prevent skeletal morbidity in patients with nonmetastatic prostate cancer receiving androgen deprivation therapy. Although the majority of and the most compelling evidence supports the use of bisphosphonates for preventing and treating androgen deprivation therapy induced bone loss, further study is needed to define the optimal regimen, timing of initiation and duration of therapy as well as long-term efficacy and safety.
我们回顾了接受雄激素剥夺治疗的非转移性前列腺癌患者骨质流失的发病机制、诊断、患病率、预防和治疗。
利用PubMed进行全面的文献检索，以确定关于接受雄激素剥夺治疗的非转移性前列腺癌患者骨矿物质密度流失的文章。对相关文章进行了回顾和评估。
骨矿物质密度流失和相关骨折最近被确认为与雄激素剥夺治疗相关的重大不良事件。接受雄激素剥夺治疗的非转移性前列腺癌患者每年骨矿物质密度流失0.6%至4.6%，在治疗的第1年内流失最为显著。除补充钙和维生素D外，目前针对雄激素剥夺治疗引起的骨质流失的治疗选择包括合成雌激素、选择性雌激素受体调节剂和双膦酸盐。最近发现了一些安全问题，包括静脉注射双膦酸盐导致的肾功能不全以及口服和静脉注射双膦酸盐导致的颌骨坏死。然而，在这种情况下，报告的肾功能不全情况极少，且未出现颌骨坏死病例。
由于骨矿物质密度流失在雄激素剥夺治疗的第1年内最为显著，且健康男性的大多数骨折发生在无骨质疏松症的人群中，因此有必要进行早期干预，以预防接受雄激素剥夺治疗的非转移性前列腺癌患者的骨骼疾病。尽管大多数且最有说服力的证据支持使用双膦酸盐预防和治疗雄激素剥夺治疗引起的骨质流失，但仍需要进一步研究来确定最佳治疗方案、开始治疗的时间和疗程以及长期疗效和安全性。
