Skip Navigation



Rheumatology Advance Access published online on October 5, 2009

Rheumatology, doi:10.1093/rheumatology/kep306
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Rider, T. G.
Right arrow Articles by Jordan, K. M.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rider, T. G.
Right arrow Articles by Jordan, K. M.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2009. 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

The modern management of gout

Tom G. Rider1 and Kelsey M. Jordan1

1Royal Sussex County Hospital, Brighton and Sussex University Hospitals NHS Trust, Brighton, UK.

Correspondence to: Kelsey M. Jordan, Royal Sussex County Hospital, Brighton and Sussex University Hospitals NHS Trust, Eastern Road, Brighton, BN2 5BE, UK. E-mail: kelsey.jordan{at}bsuh.nhs.uk


   Abstract

Gout is an inflammatory arthritis characterized by self-limiting but excruciatingly painful acute attacks. These are a consequence of monosodium urate (MSU) crystals being deposited within articular or periarticular tissue. Chronic tophaceous gout can develop after years of acute intermittent gout. Recent discoveries, including the role of the inflammasome and intracellular events demonstrating that pro-inflammatory cytokines, IL-1β, -8 and TNF-{alpha}, promote neutrophil influx genetic advances with the identification of the URAT-1 transporter and genetic variation in SLC 2A9 as a key regulator of urate homoeostasis, have given us deeper understanding of the pathophysiology of gout, and also allow for more targeted treatments. Hopefully, new and emerging therapeutic options will reduce treatment-resistant gout in patients who are unresponsive or unable to take traditional urate lowering therapy. The development of new therapies may also increase patient numbers being treated in the specialist setting, which may have several secondary benefits.

KEY WORDS: Gout, Hyperuricaemia, Treatment, Allopurinol, Febuxostat, Benzbromarone, Inflammasome, URAT-1

Submitted 10 June 2009; revised version accepted 14 August 2009.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.