Abstract
Denosumab is a potent antiresorptive agent that substantially increases bone mineral density and reduces fracture rates at all skeletal sites for as long as it is administered. However, its favorable skeletal effects reverse quickly upon its discontinuation, because of a vast increase of osteoclast number and activity, which leads to a subsequent profound increase of bone turnover above pre-treatment values, a phenomenon commonly described as “rebound phenomenon”. More importantly, most patients experience rapid, profound bone loss due to this burst of bone resorption that may lead in a minority of these patients to occurrence of fractures, especially multiple vertebral fractures. Therefore, subsequent antiresorptive treatment is mandatory, although the optimal regimen is yet to be clarified. In the present review, we outline what is currently known regarding the negative effects of denosumab discontinuation on different aspects of bone status, the factors that may affect them, and strategies to prevent them.
Highlights
Denosumab is a potent antiresorptive agent that substantially increases bone mineral density and reduces fracture rates at all skeletal sites for as long as it is administered
We summarize the most recent evidence regarding the negative effects of Dmab discontinuation on different aspects of bone status, the factors that may affect them, and strategies to prevent them
Reports from single centers who monitored their patients following the completion of the pivotal denosumab trials (FREEDOM and its Extension) concluded that the rate and amount of bone loss might be predicted by the total duration of Dmab use: patients treated for a longer period had more pronounced bone mineral density (BMD) loss at all skeletal sites [23,33]
Summary
Unit of Endocrinology and Diabetes, Campus Bio-Medico University, 00128 Rome, Italy;
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