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Ann Rheum Dis doi:10.1136/annrheumdis-2013-205036
  • Clinical and epidemiological research
  • Extended report

Zoledronate for prevention of bone erosion in tophaceous gout: a randomised, double-blind, placebo-controlled trial

  1. Ian R Reid1
  1. 1Department of Medicine, University of Auckland, Auckland, New Zealand
  2. 2Department of Radiology, Auckland District Health Board, Auckland, New Zealand
  3. 3Department of Anatomy with Radiology, University of Auckland, Auckland, New Zealand
  4. 4Department of Molecular Medicine, University of Auckland, Auckland, New Zealand
  1. Correspondence to Dr Nicola Dalbeth, Bone and Joint Research Group, Department of Medicine, Faculty of Medical and Health Sciences, University of Auckland, 85 Park Rd, Grafton, Auckland 1023, New Zealand; n.dalbeth{at}auckland.ac.nz
  • Received 8 December 2013
  • Revised 2 January 2014
  • Accepted 3 January 2014
  • Published Online First 17 January 2014

Abstract

Objectives The osteoclast has been implicated in development of bone erosion in gout. The aim of this study was to determine whether zoledronate, a potent antiosteoclast drug, influences bone erosion in people with tophaceous gout.

Methods This was a 2-year, randomised, double-blind, placebo-controlled trial of 100 people with tophaceous gout. Participants were randomised to annual administration of 5 mg intravenous zoledronate or placebo. The primary endpoint was change in the foot CT bone erosion score from baseline. Secondary endpoint was change in plain radiographic damage scores. Other endpoints were change in bone mineral density (BMD), bone turnover markers and the OMERACT-endorsed core domains for chronic gout studies.

Results There was no change in CT erosion scores over 2 years, and no difference between the two treatment groups at Year 1 or 2 (p(treat)=0.10, p(time)=0.47, p(treat*time)=0.23). Similarly, there was no change in plain radiographic scores over 2 years, and no difference between the two groups at Year 1 or 2. By contrast, zoledronate increased spine, neck of femur, total hip and total body BMD. Zoledronate therapy also reduced the bone turnover markers P1NP and β-CTX compared with placebo. There was no difference between treatment groups in OMERACT-endorsed core domains.

Conclusions Despite improvements in BMD and suppression of bone turnover markers, antiosteoclast therapy with zoledronate did not influence bone erosion in people with tophaceous gout. These findings suggest a disconnect between responses in the healthy skeleton and at sites of focal bone erosion in tophaceous gout.

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