德诺苏马布
雄激素剥夺疗法
医学
前列腺癌
骨矿物
骨质疏松症
骨重建
选择性雌激素受体调节剂
唑来膦酸
内科学
雌激素
颌骨骨坏死
骨密度保护剂
骨小梁评分
癌症
健骨
肿瘤科
内分泌学
双膦酸盐
雌激素受体
乳腺癌
定量计算机断层扫描
作者
Anna Maria Formenti,Alberto Dalla Volta,Luigi di Filippo,Alfredo Berruti,Andrea Giustina
标识
DOI:10.1016/j.tem.2020.12.004
摘要
Medical treatment of prostate cancer (PC) is multidisciplinary, resulting in prolonged survival. Androgen-deprivation therapy (ADT) can have negative effects on skeletal metabolism, particularly if combined with glucocorticoids. We discuss the pathophysiology and effects of ADT and glucocorticoids on skeletal endpoints, as well as the awareness and management of bone fragility. Coadministration of glucocorticoids is necessary with abiraterone because this causes a novel acquired form of 17-hydroxylase deficiency and synergistically increases the risk of fracture by affecting bone quality. Bone antiresorptive agents [selective estrogen receptor modulators (SERMS), bisphosphonates, and denosumab] increase bone mineral density (BMD) and in some instances reduce fracture risk in PC patients on ADT. Awareness and management of bone health in PC can be improved by integrating endocrinologists into the multidisciplinary PC team.
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