Rapid Loss of Hip Fracture Protection After Estrogen Cessation: Evidence From the National Osteoporosis Risk Assessment

Yates, John; Barrett‐Connor, Elizabeth; Barlas, Suna; Chen, Ya-Ting; Miller, Paul D.; Siris, Ethel S.

doi:10.1097/01.aog.0000114986.14806.37

Cited by 88 publications

(45 citation statements)

References 21 publications

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“…72,73,108,133 The antiresorptive drugs appear to be safe up to 5, 72,73 7, 109 8, 91 and 10 years 134 for HT, risedronate, raloxifene, and alendronate, respectively. Except for a rapid loss of hip fracture protection after estrogen discontinuation, 135 no fracture data are available after discontinuation of any of the other antiresorptive drugs.…”

Section: Length Of Therapymentioning

confidence: 99%

Canadian Consensus Conference on Osteoporosis, 2006 Update

Brown¹,

Fortier²,

Frame

et al. 2006

Journal of Obstetrics and Gynaecology Canada

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Objective-To provide guidelines for the health care provider on the diagnosis and clinical management of postmenopausal osteoporosis.Outcomes-Strategies for identifying and evaluating high-risk individuals, the use of bone mineral density (BMD) and bone turnover markers in assessing diagnosis and response to management, and recommendations regarding nutrition, physical activity, and the selection of pharmacologic therapy to prevent and manage osteoporosis. Values-The quality of evidence is rated using the criteria described in the report of the Canadian Task Force on the Periodic Health Examination. Recommendations for practice are ranked according to the method described in this report.

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Section: Length Of Therapymentioning

confidence: 99%

Canadian Consensus Conference on Osteoporosis, 2006 Update

Brown¹,

Fortier²,

Frame

et al. 2006

Journal of Obstetrics and Gynaecology Canada

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“…Similar patterns in BMD and bone turnover marker changes have been observed in the first year after withdrawal of estrogen therapy, with a return of bone turnover markers to near baseline within 2 years after estrogen discontinuation [Wasnich et al 2004;Sornay-Rendu et al 2003;Gallagher et al 2002;Greenspan et al 2002;]. It is reassuring to note that the transient increase in bone remodeling after discontinuation of estrogen therapy has not resulted in clear evidence of increased fracture risk in several large studies [Banks et al 2004;Yates et al 2004;BarrettConnor et al 2003;Cauley et al 1995]. …”

Section: Efficacymentioning

confidence: 70%

Denosumab in postmenopausal osteoporosis: what the clinician needs to know

Lewiecki

2009

Therapeutic Advances in Musculoskeletal

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Denosumab is a subcutaneously (SC) administered investigational fully human monoclonal antibody to receptor activator of nuclear factor-kB ligand (RANKL), a cytokine member of the tumor necrosis factor family that is the principal mediator of osteoclastic bone resorption. RANKL stimulates the formation, activity, and survival of osteoclasts, and is implicated in the pathogenesis of postmenopausal osteoporosis and other skeletal disorders associated with increased bone remodeling. Denosumab binds RANKL, preventing it from binding to RANK, thereby reducing the formation, activity, and survival of osteoclasts and slowing the rate of bone resorption. Postmenopausal women with low bone mineral density (BMD) treated with denosumab have a reduction of bone turnover markers and an increase in BMD that is rapid, sustained, and reversible. In postmenopausal women with osteoporosis, denosumab reduces the risk of vertebral, hip, and nonvertebral fractures. In postmenopausal women with low BMD randomized to receive denosumab or alendronate, denosumab is associated with a significantly greater increase in BMD and further reduction in bone turnover markers compared with alendronate. In postmenopausal women with low BMD who were previously treated with alendronate, those who switched to denosumab have a significantly greater BMD increase and further reduction in bone turnover markers compared with those continuing alendronate. Denosumab is well tolerated with a favorable safety profile. It is a promising emerging drug for the prevention and treatment of osteoporosis, offering a long dosing interval of every 6 months and convenient SC dosing, with the potential of improving long-term adherence to therapy compared with current oral treatments.

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“…Preliminary data do show an increase in forearm and spine quantitative computerized tomography (QCT) at QCT measured cancellous and cortical bone forearm sites [18]. This denosumab effect on cortical bone, combined with the observations that denosumab increases the two-dimensional cross-sectional area of the hip, femoral neck, and femoral shaft as measured by the parameter, hip structural analysis [19], provides evidence that denosumab increases cortical bone strength, consistent with the reduction in nonvertebral and hip fractures seen in the recent phase 3 denosumab fracture data. was a reduction in incident morphometric vertebral fracture over a 3-year period, whereas secondary end points were a reduction in hip and nonvertebral fractures and changes in BMD and BTMs.…”

Section: Anti-rankl Antibodymentioning

confidence: 92%

Denosumab: Anti-RANKL antibody

Miller

2009

Curr Osteoporos Rep

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Denosumab (anti-receptor activator of nuclear factor-kappaB ligand antibody) is a novel agent, a fully human monoclonal antibody that inhibits osteoclastic-medicated bone resorption by binding to osteoblast-produced RANKL. By reducing RANKL binding to the osteoclast receptor RANK, bone resorption and turnover decrease. In phase 2 dose-ranging studies, denosumab had a rapid onset and offset effect. Also, in patients who had received 2 years of denosumab and were discontinued for the third year, rechallenge with denosumab during the fourth year demonstrated a return of responsiveness to denosumab that mimicked the initial treatment. Phase 3 pivotal fracture data were recently presented with positive outcome data; denosumab (60 mg subcutaneously every 6 months) significantly reduced vertebral, nonvertebral, and hip fracture risk compared with placebo, and had an excellent safety profile through 3 years of use. Denosumab will offer a novel approach to managing postmenopausal osteoporosis, one that should be associated with a high adherence rate and global fracture risk reduction.

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Rapid Loss of Hip Fracture Protection After Estrogen Cessation: Evidence From the National Osteoporosis Risk Assessment

Abstract: II-2

Cited by 88 publications

References 21 publications

Canadian Consensus Conference on Osteoporosis, 2006 Update

Canadian Consensus Conference on Osteoporosis, 2006 Update

Denosumab in postmenopausal osteoporosis: what the clinician needs to know

Denosumab: Anti-RANKL antibody

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