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Rheumatology Advance Access published online on December 24, 2008
Rheumatology, doi:10.1093/rheumatology/ken460
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© The Author 2008. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Review

Crystal ball gazing: new therapeutic targets for hyperuricaemia and gout

N. Dalbeth1 and T. Merriman2

1Department of Medicine, Faculty of Medical and Health Sciences, University of Auckland, Auckland and 2Department of Biochemistry, University of Otago, Dunedin, New Zealand.

Correspondence to: N. Dalbeth, Department of Medicine, Faculty of Medical and Health Sciences, University of Auckland, 85 Park Rd, Grafton, Private Bag 92019, Auckland, New Zealand. E-mail: n.dalbeth{at}auckland.ac.nz


  Abstract

Recent studies in diverse disciplines have led to significant advances in the understanding of the basic biology of hyperuricaemia and gout, with important implications for future treatment. These findings include genetic variation within SLC2A9 as a key regulator of urate homeostasis, and identification of urate–anion exchanger urate transporter 1 (URAT1) and other renal uric acid transporters. Recognition of urate as an endogenous danger signal and activator of the adaptive immune response suggests an important role for urate crystals in non-microbial immune surveillance. The central role of NALP3 inflammasome activation and IL-1β signalling in the initiation of the acute gout attack raises the possibility of new therapeutic targets. Disordered osteoclastogenesis in patients with chronic gout highlights potential therapies for prevention of joint damage. This review summarizes these findings and the potential relevance for future management of gout.

KEY WORDS: Gout, Hyperuricaemia, Genetics, Inflammation, Treatment

Submitted 28 August 2008; Accepted 18 November 2008


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