Haeri Nami Safai, Perera Subashan, Greenspan Susan L
Division of Geriatric Medicine, Department of Medicine, University of Pittsburgh, 3471 Fifth Ave, Suite 1110, Pittsburgh, PA, 15213, USA.
Division of Endocrinology and Metabolism, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA.
Calcif Tissue Int. 2025 Mar 27;116(1):55. doi: 10.1007/s00223-025-01364-y.
Discontinuation of denosumab can result in rebound bone loss and increased vertebral fracture risk. In residents of long-term care communities (LTCCs) with osteoporosis, there is limited data on managing the risks after discontinuation. We investigated the impact of a single dose of zoledronic acid on bone density and microarchitecture following two years of denosumab treatment. In an open-label, one-year extension study following a two-year double-blind, placebo-controlled, randomized clinical trial, 39 older adults aged 65 years and above, who were residents of LTCCs and participants in the PROUD (PReventing Osteoporosis Using Denosumab) trial, received a single 5 mg dose of zoledronic acid after completing four doses of denosumab 60 mg during the PROUD trial. We aim to evaluate the effects of a single 5 mg dose of zoledronic acid on bone mineral density (BMD) at the lumbar spine, total hip, femoral neck, and one-third radius, as well as on the spine trabecular bone score (TBS), over a one-year period. Additionally, we surveyed patients for fractures. Our study included 27 women and 12 men, with a mean age of 81.5 years. Twelve months after the administration of zoledronic acid, the mean percent changes from the end of the denosumab trial showed no significant decline in any of the BMD sites in both women and men. In women, the mean percent changes were as follows: spine 0.97 (95% CI: -0.7 to 2.7, p = 0.242) and total hip -0.10 (95% CI: -2.3 to 2.1, p = 0.927). In men, the changes were -0.32 (95% CI: -3.7 to 3.1, p = 0.832) for the spine and 1.79 (95% CI: -0.7 to 4.3, p = 0.139) for the total hip. These findings indicate no evidence of rebound bone loss. In women, TBS significantly increased by 3.9% (95% CI: 0.8 to 5.8, p = 0.007), suggesting improved bone microarchitecture. In men, there was a trend toward improvement in TBS, with an increase of 3.3% (95% CI: -4.0 to 13.0, p = 0.054). There were no reported fragility fractures among participants during the post-denosumab period. In residents of LTCCs with osteoporosis receiving a single 5 mg dose of zoledronic acid following two years of denosumab, we found no evidence of a loss in BMD or TBS. Further, participants experienced enhanced bone microarchitecture.
停用地诺单抗可导致骨量反弹流失，并增加椎体骨折风险。在患有骨质疏松症的长期护理社区（LTCC）居民中，关于停用后风险管理的数据有限。我们研究了单剂量唑来膦酸对接受两年地诺单抗治疗后的骨密度和骨微结构的影响。在一项为期两年的双盲、安慰剂对照、随机临床试验后的开放标签、为期一年的延长期研究中，39名65岁及以上的老年人，他们是LTCC的居民且是PROUD（使用地诺单抗预防骨质疏松症）试验的参与者，在PROUD试验中完成四剂60mg地诺单抗后，接受了一剂5mg的唑来膦酸。我们旨在评估单剂量5mg唑来膦酸在一年时间内对腰椎、全髋、股骨颈和桡骨远端三分之一处的骨矿物质密度（BMD）以及对脊柱小梁骨评分（TBS）的影响。此外，我们对患者进行了骨折情况调查。我们的研究包括27名女性和12名男性，平均年龄为81.5岁。在给予唑来膦酸12个月后，与地诺单抗试验结束时相比，女性和男性的任何BMD部位的平均百分比变化均未显示出显著下降。在女性中，平均百分比变化如下：脊柱0.97（95%CI：-0.7至2.7，p = 0.242）和全髋-0.10（95%CI：-2.3至2.1，p = 0.927）。在男性中，脊柱的变化为-0.32（95%CI：-3.7至3.1，p = 0.832），全髋的变化为1.79（95%CI：-0.7至4.3，p = 0.139）。这些结果表明没有骨量反弹流失的证据。在女性中，TBS显著增加了3.9%（95%CI：0.8至5.8，p = 0.007），表明骨微结构得到改善。在男性中，TBS有改善的趋势，增加了3.3%（95%CI：-4.0至13.0，p = 0.054）。在接受地诺单抗治疗后的时期内，参与者中没有报告脆性骨折。在接受两年地诺单抗治疗后再接受单剂量5mg唑来膦酸的LTCC骨质疏松症居民中，我们没有发现BMD或TBS丢失的证据。此外参与者的骨微结构得到了改善。
