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THU0458 Influence of Oral Prednisolone on Effect of Denosumab on Osteoporosis in Patients with Japanese Rheumatoid Arthritis; 12 Months of Follow-Up – A Multicenter Registry Study
  1. Y. Kanayama1,
  2. Y. Hirano2,
  3. N. Takahashi3,
  4. S. Asai3,
  5. N. Ishiguro3,
  6. T. Kojima3,
  7. on behalf of TBCR-BONE Study Group
  1. 1Orthopedic Surgery and Rheumatology, Toyota Kosei Hospital, Toyota
  2. 2Rheumatology, Toyohashi Municipal Hospital, Toyohashi
  3. 3Orthopedic Surgery, Nagoya University Graduate School of Medicine, Nagoya, Japan

Abstract

Background Denosumab (DMB) is a fully human monoclonal antibody to the receptor activator of nuclear factor-kappaB ligand (RANKL) that blocks its binding RANK, inhibiting the development and activity of osteoclasts, decreasing bone resorption, increasing bone density and reducing fracture risk. Osteoporosis (OP) is more frequent in patients with rheumatoid arthritis (RA) than in the general population due to active systemic inflammation as well as the use of glucocorticoid and immobility. However efficacy of denosmab is not clear in patirnts with glucocorticoid- induced OP in RA. Therefore we investigated the influence of oral prednisolone on effect of DMB in patients with Japanese RA from initiation to 12 months at this time.

Objectives This prospective study investigated the efficacy of DMB for 12 months on glucocorticoid- induced OP in RA patients.

Methods Patients with a diagnosis of RA according to the 2010 ACR/EULAR criteria who had been prescribed DMB from Tsurumai Biologics Communication Registry (TBCR)-BONE between October 2013 and October 2014 were enrolled. The final study cohort of 67 patients received continuous DMB therapy more than 12 months. The DMB dose was 60mg at once every 6 months. In all cases native or activated vitamin D has been used. We reviewed the results for 6 and 12 months about the increase and decrease of bone mineral density (BMD) of lumbar spine (LS) and total hip (TH) by DEXA and bone turnover markers, intact n-terminal propeptide type I procollagen (PINP) and tartrate-resistant acid phopshatate form 5b (TRACP-5b)

Results In the patients receiving oral prednisolone group (n=26, R-PSL) and not receiving group (n=41, N-PSL), the number of female was each 24 (92%) and 40 (98%) cases (p=0.555). The mean age was 68.5 ± 7.9 and 69.9 ± 7.2 years old (p=0.657); disease duration was 16.3 ± 9.9 and 16.0 ± 13.3 years (p=0.532); the body mass index was 19.9 ± 3.5 and 19.6 ± 2.9 (p=0.852) and the FRAX was 32.7 ± 18.3 and 21.6 ± 13.5 (p=0.007). Clinical findings related to RA and OP at baseline were as follows; CRP 1.1 ± 1.3 and 0.4 ± 1.0 mg/dl (p=0.017); DAS-CRP 3.20 ± 1.13 and 2.39 ± 1.22 (p=0.003); m-HAQ 1.20 ± 0.83 and 0.73 ± 0.72 (p=0.026); PINP 60.4 ± 37.0 and 55.0 ± 32.7 μg/l (p=0.433); TRACP-5b 502 ± 245 and 488 ± 206 mU/dL (p=0.852); LS-BMD 0.86 ± 0.18 and 0.83 ± 0.17 g/cm2(p=0.296) and TH-BMD 0.60 ± 0.11 and 0.60 ± 0.08 g/cm2 (p=0.892). The rate of decreased PINP from baseline to 6 and 12 months were each -29.4% vs -40.2% (p=0.289) at 6 month and -13.7% vs -41.4% (p=0.118) at 12month and TRAC-5b were -28.5% vs -35.1% (p=0.849) at 6 month and -21.4% vs -31.6% (p=0.401) at 12month in the R-PSL group vs N-PSL group. The rate of increased LS-BMD from baseline to 6 and 12 months were each 3.4% vs 4.5% (p=0.305) at 6 month and 4.7% vs 6.8% (p=0.175) at 12month and TH-BMD were 3.0% vs 3.0% (p=0.816) at 6 month and 3.9% vs 3.9% (p=0.898) at 12month in the R-PSL group vs N-PSL group (Fig. 1). The rate of patients who did not increase LS-BMD and TH-BMD for 12 months were each 17.4% vs 15.4% (p=0.836) and 17.4% vs 5.0% (p=0.179) in the R-PSL group vs N-PSL group (Fig. 2).

Conclusions DMB was effective in OP of RA patients. Oral prednisolone use did not influence the efficacy of DMB in the short period of 6 and 12 months.

Disclosure of Interest Y. Kanayama: None declared, Y. Hirano Speakers bureau: Abbvie Japan, Eisai, Mitsubishi Tanabe Pharma, Pfizer, Chugai Pharmaceutical, and Bristol-Myers Squibb., N. Takahashi Speakers bureau: Abbvie Japan Co. Ltd, Eisai Co. Ltd, UCB Japan Co. Ltd, Mitsubishi Tanabe Pharma Corporation, Takeda Pharmaceutical Company Ltd, Pfizer Co. Ltd, Chugai Pharmaceutical Co. Ltd, Janssen Pharmaceutical K.K., and Bristol-Myers Squibb Co. Ltd., S. Asai: None declared, N. Ishiguro Grant/research support from: Daiichi Sankyo, Takeda Pharmaceutical, Hisamitsu Pharmaceutical, Otsuka Pharmaceutical, Taisho Toyama Pharmaceutical, Kaken Pharmaceutical, Eisai, Janssen Pharmaceutical, Bristol-Myers Squibb, AbbVie, ChugaiPharmaceutical, Mitsubishi Tanabe Pharmaceutical, Astellas Pharma, and Pfizer Japan, Speakers bureau: Daiichi Sankyo, Takeda Pharmaceutical, Hisamitsu Pharmaceutical, Otsuka Pharmaceutical, Taisho Toyama Pharmaceutical, Kaken Pharmaceutical, Eisai, Janssen Pharmaceutical, Bristol-Myers Squibb, AbbVie, Chugai Pharmaceutical, MitsubishiTanabe Pharmaceutical, Astellas Pharma, and Pfizer Japan., T. Kojima Speakers bureau: Mitsubishi Tanabe Pharma, Takeda Pharma, Eisai Pharma, AbbVie, Bristol-Myers Squibb, and Pfizer, Janssenn Pharmaceutical Companies, Astellas Pharma and Chugai Pharma.

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