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THU0494 The efficacy of denosumab in glucocorticoid-induced osteoporosis did not depend on prior treatment but was affected by the dosage of glucocorticoid
  1. N. Iwamoto1,
  2. Y. Ueki2,
  3. T. Aramaki2,
  4. K. Ichinose1,
  5. K. Eguchi2,
  6. A. Kawakami1
  1. 1Department of Immunology and Rheumatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki
  2. 2Department of Rheumatology, Sasebo Chuo Hospital, Sasebo, Japan


Background Despite of the good clinical efficacy of denosumab for primary osteoporosis, 2017 American College of Rheumatology guideline for treatment of glucocorticoid-induced osteoporosis (GIOP) placed denosumab as second-line treatment because of lack of clinical experiences with concomitantly use of immunosuppressive agents. Moreover, recently large phase 3 study in primary osteoporosis revealed that transition from teriparatide to denosumab continuously increased bone mineral density (BMD)1 However, there is still remain unclear whether prior treatment affect to the efficacy of denosumab in GIOP.

Objectives The aim of this study is to compare the therapeutic effect of denosumab in GIOP between previous anti-osteoporotic treatments, and to investigate the factor that influence the efficacy of denosumab in GIOP.

Methods Sixty-six patients for whom treated by denosumab, were enrolled. All patients were receiving several dosages of predonisolone (PSL) (2–20 mg) for RA and connective tissue diseases at initiation of denosumab. 23 patients had been treated with daily teriparatide and 27 patients had been treated with bisphosphonate (BPs) prior to denosumab. The rest 16 patients had not been treated by anti-osteoporosis medication at initiation of denosumab. We evaluated BMD at lumbar spine and bone turnover markes (NTX, BAP and P1NP) every 6 months for 12 months. The changes in BMD was compared among these 3 groups at 6 months and at 12 months. To assess the factors which influences clinical response of denosumab in GIOP, univariate and multivariable ordinal logistic regression analyses were used.

Results Mean percentage change in BMD of lumbar spine from baseline to 6 and 12 months were significant (2.85% increased; p<0.0001% and 4.40% increased; p<0.0001, respectively) Gains higher than 3% were observed in 68.2%. Whereas, the subjects who showed decrement of BMD at 12 months were few (16.67%). All bone turnover markers determined in this study were decreased at 6 months. Transition from BPs to denosumab further increase BMD at 12 months as compared to transition from teriparatide to denosumab (4.71% increased, 3.71% increased, respectively). However, difference among these 2 groups was not significant and furthermore, the changes in BMD in patients who did no transition from anti-osteoporosis medication to denosumab also showed no significant difference (figure 1). Univariate analysis showed that dosage/duration of PSL, body weight and gender were associated with BMD increase higher than 3% at 12 months. Among these candidates, multivariable logistic analysis showed that dose of PSL was independently associated with clinical response of denosumab (OR 1.36, 95% CI 1.045–1.761 P<0.01). No hypocalcemia and osteonecrosis of the jaw was observed during the study period.

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Conclusions Our present study demonstrated that denosumab increased BMD in GIOP regardless of prior anti-osteoporotic treatment in ‘real-world’ settings. We should consider denosmab treatment for GIOP, especially who are treated by much dose of glucocorticoids or at the time when the efficacy of BPs is diminished.

Reference [1] Leder BZ, et al. Denosumab and teriparatide transitions in postmenopausal osteoporosis (the DATA-Switch study): extension of a randomised controlled trial. Lancet2015;386(9999):1147–55.

Disclosure of Interest None declared

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