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Management of cancer treatment-induced bone loss (CTIBL) in patients with breast cancer or prostate cancer

Journal

JOURNAL OF BONE AND MINERAL METABOLISM
Volume 41, Issue 3, Pages 307-316

Publisher

SPRINGER JAPAN KK
DOI: 10.1007/s00774-023-01414-1

Keywords

Breast cancer; Prostate cancer; Cancer-therapy induced bone loss; Bisphosphonates; Denosumab

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Breast cancer and prostate cancer, which are dependent on sex hormones, are often treated with hormone-suppression therapies. However, these therapies can lead to bone loss and osteoporosis. Current evidence shows that endocrine therapy decreases bone mineral density, aromatase inhibitors increase fractures in breast cancer patients, and androgen deprivation therapy is likely to increase fractures in prostate cancer patients. Administering bisphosphonates, denosumab, and SERMs can increase bone mass in patients on hormone therapy for breast and prostate cancer, and they also reduce the risk of fractures.
Breast cancer and prostate cancer are sex hormone-dependent cancers, and estrogen or androgen suppression therapy is the standard treatment. Cancer treatment-induced bone loss (CTIBL): bone loss and osteoporosis have become important side effects of these therapies. To summarize the current evidences, (1) Endocrine therapy for breast cancer and prostate cancer is associated with a significant decrease in bone mineral density. (2) Aromatase inhibitors (AI) for breast cancer are associated with a significant increase in fractures, and androgen deprivation therapy (ADT) for prostate cancer is likely to be associated with an increase in fractures. (3) Administration of bisphosphonates and denosumab increases bone mass in patients undergoing endocrine therapy for breast cancer. Administration of bisphosphonates, denosumab, and SERMs increased bone mass in patients undergoing ADT therapy for prostate cancer. (4) Bisphosphonates and denosumab reduce fracture risk in patients on AI for breast cancer, and toremifene and denosumab in patients on ADT for prostate cancer.

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