Affiliation:
1. Department of Respiratory Medicine and Clinical Immunology, Osaka University Graduate School of Medicine
2. Laboratory of Immunopathology, World Premier International Immunology Frontier Research Center
3. Integrated Frontier Research for Medical Science Division, Institute for Open and Transdisciplinary Research Initiatives, Osaka University, Suita, Osaka, Japan
Abstract
Abstract
Objective
Prevention of steroidal osteoporosis is an important issue. There is no clear consensus on the impact of anti-RANKL antibody (denosumab) on BMD in patients with glucocorticoid-induced osteoporosis (GIO). In this study, we aimed to evaluate the impact of denosumab on BMD loss in patients with GIO.
Methods
A comprehensive systematic review and meta-analysis was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guidelines. PubMed, Web of Science and Google Scholar were used to search for original studies reported about BMD in patients with GIO treated with denosumab. In meta-analysis of BMD, the mean difference in the rate of change from baseline and the 95% CI were calculated using the random effects model. The mean differences in patients treated with denosumab were compared with those in patients treated with bisphosphonates.
Results
Out of 713 studies identified, seven studies met the selection criteria for the meta-analysis. At 6 and 12 months of denosumab therapy, increases in BMD were observed in the lumbar spine (2.99% [95% CI 2.71, 3.28] and 4.59% [95% CI 4.17, 5.01]), total hip (1.34% [95% CI 0.64, 2.04] and 2.16% [95% CI 2.05, 2.27]) and femoral neck (0.12% [95% CI −0.38, 0.62] and 1.55% [95% CI 0.45, 2.65]). Additionally, denosumab resulted in significant increases in BMD in the lumbar spine and femoral neck at 12 months compared with bisphosphonate therapy.
Conclusion
Patients with GIO experienced significant increases in BMD in response to treatment with denosumab that were detected in the lumbar spine, total hip and femoral neck at 12 months.
Publisher
Oxford University Press (OUP)
Cited by
13 articles.
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