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Randomized Controlled Trial
. 2018 Mar 15;13(3):e0193846.
doi: 10.1371/journal.pone.0193846. eCollection 2018.

The effects of denosumab and alendronate on glucocorticoid-induced osteoporosis in patients with glomerular disease: A randomized, controlled trial

Ken Iseri  1   2 , Masayuki Iyoda  1 , Makoto Watanabe  1   2 , Kei Matsumoto  1 , Daisuke Sanada  1 , Takashi Inoue  1 , Shohei Tachibana  1 , Takanori Shibata  1
Affiliations
Randomized Controlled Trial

The effects of denosumab and alendronate on glucocorticoid-induced osteoporosis in patients with glomerular disease: A randomized, controlled trial

Ken Iseri et al. PLoS One. .

Abstract

Introduction: The clinical utility of denosumab for the treatment of glucocorticoid-induced osteoporosis (GIOP) has yet to be established. This study aimed to compare the effects of denosumab on bone mineral density (BMD) and bone turnover markers to those of alendronate in patients with GIOP.

Methods: A prospective, single-center study of 32 patients (18 men; median age, 66.0 years) with glomerular disease receiving prednisolone (PSL) who were diagnosed as having GIOP and had not received bisphosphonates before was conducted. Participants were randomized to either alendronate (35 mg orally once a week) or denosumab (60 mg subcutaneously once every 6 months), and all subjects received calcitriol. The primary endpoint was the percent change in lumbar spine (LS) BMD at 12 months of treatment.

Results: The demographic and clinical characteristics at baseline were not significantly different between the groups. Denosumab treatment markedly decreased serum levels of t-PINP, BAP, and TRACP-5b at 12 months compared to baseline (-57.4%, p<0.001; -30.9%, p<0.01; -57.7%, p<0.001, respectively). After 12 months of alendronate treatment, serum levels of t-PINP, BAP, and TRACP-5b were also significantly decreased compared to pretreatment (-38.9%, p<0.01; -16.3%, p<0.05; -43.5%, p<0.01, respectively). However, no significant differences in the changes of bone turnover markers were found between the two groups. As for the effects on BMD, denosumab treatment markedly increased LS BMD from 6 months compared to baseline, whereas no significant difference compared to pretreatment was found in the alendronate group during the study period. In the comparison of the two groups, a large increase of LS BMD was found in the denosumab treatment group compared to the alendronate treatment group at 12 months (p<0.05).

Conclusions: In patients with GIOP, denosumab treatment markedly suppressed bone turnover, which led to a significantly greater increase in LS BMD than with alendronate treatment. These results suggest that denosumab is a therapeutic option for the treatment of GIOP.

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Conflict of interest statement

Competing Interests: T.S. received grants from Daiichi Sankyo Co., Ltd. and Teijin Pharma Ltd. However, these corporations were not involved in designing or conducting this study. No other authors have any conflicts of interest to declare.

Figures

Fig 1
Fig 1. Patient disposition.
Abbreviations: FAS, full analysis set.
Fig 2
Fig 2. Effects of denosumab and alendronate on bone turnover makers.
Percent changes (means ± SEM) in bone turnover markers from baseline to 12 months in the denosumab and alendronate groups. *P compared with the alendronate group (by Wilcoxon’s rank sum test). #P compared with baseline (by Wilcoxon’s signed rank test). Abbreviations: TRACP-5b, tartrate-resistant acid phosphatase 5b; BAP, bone-specific alkaline phosphatase; t-PINP, total-type I collagen N-terminal propeptide.
Fig 3
Fig 3. Effects of denosumab and alendronate on BMD.
Percent changes (mean ± SEM) in bone mineral density from baseline to 12 months in the lumbar spine (A), femoral neck (B), and ultra-distal radius (C) in the denosumab and alendronate groups. *P compared with the alendronate group (by Wilcoxon’s rank sum test). #P compared with baseline (by Wilcoxon’s signed rank test).
See this image and copyright information in PMC

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