FRI0579 Influence of oral prednisolone on effect of denosumab on osteoporosis in patients with japanese rheumatoid arthritis; 24 months of follow-up ∼a multicenter registry study∼. (15th June 2017)

• Record Type: Journal Article
• Authors: Kanayama, Y; Hirano, Y; Takahashi, N; Asai, S; Ishiguro, N; Kojima, T
• Is Part Of: Annals of the rheumatic diseases. Volume 76(2017)Supplement 2
• Page Start: 708
• Page End: 708
• Publication Date: 2017-06-15
• Subjects: Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/annrheumdis-2017-eular.4677
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Background: Denosumab (DMB) is a fully human monoclonal antibody to the 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 DMB 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 24 months at this time. Objectives: This prospective study investigated the efficacy of DMB for 24 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 2015 were enrolled. The final study cohort of 63 patients received continuous DMB therapy more than 24 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 24 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=23, GC+) and not receiving group (n=40, GC-), the number of female was each 21 (91%) and 39 (98%) cases (p=0.548). The mean age was 69.8±7.0 and 71.0±7.3 years old (p=0.622); disease duration was 16.0±8.9 and 15.7±12.6 years (p=0.592); the body mass index was 20.7±3.5 and 19.7±3.0 (p=0.335) and the FRAX was 34.2±19.1 and 24.6±13.9 (p=0.040). Clinical findings related to RA and OP at baseline were as follows; CRP 1.2±1.4 and 0.5±1.0 mg/dl (p=0.009); DAS-CRP 3.16±1.17 and 2.50±1.27 (p=0.025); m-HAQ 1.24±0.90 and 0.82±0.82 (p=0.065); P1NP 60.1±38.6 and 56.9±33.5 μg/l (p=0.711); TRACP-5b 513±257 and 505±202 mU/dL (p=0.689); LS-BMD 0.87±0.18 and 0.80±0.14 g/cm 2 (p=0.074) and TH-BMD 0.60±0.11 and 0.59±0.08 g/cm 2 (p=0.457). The rate of decreased P1NP from baseline to 6, 12, 18 and 24 months were each -25.6% vs -41.6% (p=0.129) at 6 month, -8.0% vs -42.6% (p=0.031) at 12 month, -19.5% vs -27.5% (p=0.235) at 18 month and -13.8% vs -33.8% (p=0.134) at 24 month and TRAC-5b were -26.5% vs -38.7% (p=0.710) at 6 month, -22.0% vs -35.1% (p=0.229) at 12 month, -25.2% vs -28.1% (p=0.792) at 18 month and -20.6% vs -27.3% (p=0.663) at 24 month in the GS+ vs GS- group. The rate of increased LS-BMD from baseline to 6, 12, 18 and 24 months were each 4.1% vs 4.6% (p=0.671) at 6 month, 5.3% vs 7.0% (p=0.361) at 12 month, 8.1% vs 8.1% (p=0.438) at 18 month and 10.0% vs 7.7% (p=0.104) at 24 month and TH-BMD were 3.3% vs 2.7% (p=0.690) at 6 month, 1.4% vs 3.8% (p=0.804) at 12 month, 6.4% vs 4.0% (p=0.259) at 18 month and 5.7% vs 4.3% (p=0.945) at 24 month in the GS+ vs GS- group (Fig.1, 2). Conclusions: DMB was effective in OP of RA patients. Oral prednisolone use did not influence the efficacy of DMB for 24 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: bbvie 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, 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