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接受激素消融治疗的癌症患者的治疗相关骨丢失和骨折:地舒单抗的疗效和安全性。

Treatment-induced bone loss and fractures in cancer patients undergoing hormone ablation therapy: efficacy and safety of denosumab.

机构信息

College of Medicine, Penn State Hershey Medical Center, Hershey, PA, USA.

出版信息

Clin Med Insights Oncol. 2012;6:287-303. doi: 10.4137/CMO.S8511. Epub 2012 Aug 16.

DOI:10.4137/CMO.S8511
PMID:22933844
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3427033/
Abstract

Hormone ablation therapy (HALT) for breast or prostate cancer accelerates the development of osteoporosis in both men and women by causing estrogen deficiency, which increases the risk for fracture by promoting bone resorption mediated by osteoclasts. Denosumab, a fully human monoclonal antibody that inhibits osteoclast formation and function, increases bone mass in patients undergoing hormone ablation therapy. In the HALT study of 1,468 men with prostate cancer on androgen-deprivation therapy, denosumab significantly reduced the risk of new vertebral fractures, increased bone mineral density (BMD), and reduced markers of bone turnover. In a study of 252 women with breast cancer undergoing adjuvant aromatase inhibitor (AI) therapy, denosumab increased BMD at 12 and 24 months, overall and in all patient subgroups. The overall rates of adverse events were similar to placebo. Clinicians should consider fracture risk assessment and therapies such as denosumab to increase bone mass in patients on hormone ablation therapy who are at high risk for fracture.

摘要

激素去势治疗(HALT)可通过引起雌激素缺乏加速男性和女性的骨质疏松症的发展,这会通过促进破骨细胞介导的骨吸收增加骨折风险。地舒单抗是一种完全人源化单克隆抗体,可抑制破骨细胞的形成和功能,增加正在接受激素去势治疗的患者的骨量。在 HALT 研究中,1468 名接受雄激素剥夺治疗的前列腺癌男性中,地舒单抗显著降低了新发椎体骨折的风险,增加了骨密度(BMD),并降低了骨转换标志物。在一项接受辅助芳香化酶抑制剂(AI)治疗的 252 名乳腺癌女性的研究中,地舒单抗在 12 个月和 24 个月时增加了 BMD,总体和所有患者亚组均如此。总的不良事件发生率与安慰剂相似。临床医生应考虑骨折风险评估和治疗方法,如地舒单抗,以增加有骨折高风险的正在接受激素去势治疗的患者的骨量。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baf5/3427033/a482feb6c9b4/cmo-6-2012-287f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baf5/3427033/b4574482a4c9/cmo-6-2012-287f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baf5/3427033/252ebf2444f2/cmo-6-2012-287f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baf5/3427033/c9b1c994f080/cmo-6-2012-287f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baf5/3427033/4e1056db92cd/cmo-6-2012-287f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baf5/3427033/a482feb6c9b4/cmo-6-2012-287f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baf5/3427033/b4574482a4c9/cmo-6-2012-287f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baf5/3427033/4de5a89b608d/cmo-6-2012-287f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baf5/3427033/f21b05054829/cmo-6-2012-287f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baf5/3427033/252ebf2444f2/cmo-6-2012-287f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baf5/3427033/c9b1c994f080/cmo-6-2012-287f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/baf5/3427033/4e1056db92cd/cmo-6-2012-287f6.jpg
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