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Effects of denosumab on bone mineral density and bone turnover in patients with rheumatoid arthritis receiving concurrent glucocorticoids or bisphosphonates
  1. Robin K Dore1,
  2. Stanley B Cohen2,
  3. Nancy E Lane3,
  4. William Palmer4,
  5. William Shergy5,
  6. Lifen Zhou6,
  7. Huei Wang6,
  8. Wayne Tsuji7,
  9. Richard Newmark6
  1. 1Robin K Dore Inc, Tustin, California, USA
  2. 2Metroplex Clinical Research Center, Dallas, Texas, USA
  3. 3University of California-Davis Medical Center, Sacramento, California, USA
  4. 4William Palmer, Westroads Medical Group, Omaha, Nebraska, USA
  5. 5Rheumatology Associates of North Alabama, Huntsville, Alabama, USA
  6. 6Amgen Inc, Thousand Oaks, California, USA
  7. 7Amgen Inc, Seattle, Washington, USA
  1. Correspondence to Dr Robin K Dore, 18102 Irvine Boulevard #104, Tustin, CA 92780, USA; rkdmail{at}sbcglobal.net

Abstract

Objectives To report results of subgroup analyses of bone mineral density (BMD) and bone turnover markers from a randomised, double-blind, placebo-controlled, phase II study of denosumab, an investigational RANKL inhibitor, in patients with rheumatoid arthritis (RA) concurrently receiving treatment with bisphosphonates or glucocorticoids.

Methods Patients received subcutaneous placebo (n=75), denosumab 60 mg (n=71) or denosumab 180 mg (n=72) at baseline and 6 months. Assessments included dual x-ray absorptiometry scans of the lumbar spine and hip, and determination of levels of serum type I C-telopeptide (sCTx-I) and serum procollagen 1N-terminal peptide (P1NP).

Results Denosumab treatment increased mean lumbar spine and hip BMD and reduced sCTx-I and P1NP compared with placebo through 12 months, regardless of baseline BMD or marker levels or concomitant bisphosphonate or glucocorticoid use.

Conclusions This study extends evidence that denosumab increases BMD and reduces bone turnover in patients with RA and may provide a new therapeutic option for reducing systemic bone loss in patients with RA.

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Footnotes

  • Funding This study was funded by Amgen Inc. RKD has received research grants from Amgen, Merck, Eli Lilly and Roche. She has received consulting fees from Merck, Eli Lilly, Roche, UCB and Novartis and has been on the speakers' bureau for Merck, Eli Lilly, Roche, Procter & Gamble, Pfizer, Sanofi-Aventis and Novartis. SBC has received research grants and consulting fees from Amgen, Genentech, Biogen-IDEC, Merck, Sanofi-Aventis, Procter & Gamble, Pfizer, Centocor, Scios, Bristol Myers Squibb and Wyeth-Ayerst. NEL has received research grants and consulting fees from Proctor and Gamble, Merck and Co, Eli Lilly, Amgen, ZosanoPharma and Pfizer. WP has received research grants and/or consulting fees and/or served on speakers' bureaus for Pfizer, Genentech Inc, Bristol Myers Squibb, Wyeth, Roche, TAP, Abbott, Centocor and Amgen Inc.

  • Competing interests WS has served on speakers' bureaus for Amgen Inc, Centocor, Abbott, Bristol-Meyers Squibb and Genentech. LZ, HW, WT and RN are employees of Amgen and have received Amgen stock and stock options.

  • Ethics approval Approval was obtained from the institutional review boards and independent ethics committees of participating medical centres.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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