抗骨质疏松症药物与降低癌症患者死亡率

M. Chandran, Tang Ching Lau
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摘要

骨质疏松症和癌症之间有着复杂的关系,每种疾病都会影响另一种疾病的进展和结果。1 多种因素,如化疗和激素疗法,以及恶性细胞对骨组织的直接侵袭,都会导致癌症患者骨质流失加速。各种抗骨质疏松症药物,包括双膦酸盐、地诺苏单抗和选择性雌激素受体调节剂(SERMs)等抗骨质吸收药物,以及特立帕肽和罗莫索单抗等同化制剂,在非癌症人群中均具有预防骨质流失和降低骨折风险的疗效。这些药物通过不同的机制产生作用,如抑制破骨细胞活性、调节激素途径或促进骨形成。2 然而,这些药物对癌症患者的疗效仍是一个持续研究和争论的领域。癌症相关骨质流失与抗骨质疏松药物的作用和潜在益处之间的相互作用十分复杂。抗骨质疏松症药物对骨质疏松性骨折的癌症患者有明显疗效,其合理的生物学机制值得探讨。除了对骨密度的直接影响外,这些药物还可能影响肿瘤微环境、免疫反应以及影响癌症进展的因子的释放。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Anti-osteoporosis drugs and reduction of mortality in cancer patients
Osteoporosis and cancer share a complex relationship, with each condition influencing the progression and outcomes of the other.1 Multiple factors, such as chemo- and hormonal therapies, and the direct invasion of bone tissue by malignant cells contribute to the accelerated bone loss seen in cancer patients.1 Various anti-osteoporosis drugs, including anti-resorptives such as bisphosphonates, denosumab and selective estrogen receptor modulators (SERMs), and anabolic agents such as teriparatide and romosozumab have demonstrated efficacy in preventing bone loss and reducing fracture risk in non-cancer populations. These medications exert their effects through different mechanisms, such as inhibiting osteoclast activity, modulating hormonal pathways or promoting bone formation.2 However, their effectiveness in cancer patients remains an area of ongoing research and debate. The interplay between cancer-related bone loss and the actions and potential benefits of anti-osteoporosis drugs is complex. The plausible biological mechanisms underlying the observed benefits of anti-osteoporosis drugs in cancer patients with osteoporotic fractures warrant exploration. Beyond their direct effects on bone density, these medications may influence the tumour microenvironment, immune response, and the release of factors that affect cancer progression.1,3
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