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Annals of the Rheumatic Diseases 2007;66:1269-1270; doi:10.1136/ard.2007.078469
Copyright © 2007 BMJ Publishing Group Ltd & European League Against Rheumatism.

EDITORIAL

Why is gout so poorly managed?

Eliseo Pascual1, Francisca Sivera2

1 Professor of Medicine (Rheumatology), Hospital General Universitario de Alicante, Universidad Miguel Hernández, Alicante, Spain
2 Staff Rheumatologist, Hospital General Universitario de Alicante, Alicante, Spain

Correspondence to:
Professor Eliseo Pascual, Sección de Reumatología, Hospital General Universitario de Alicante, Maestro Alonso 109, 03010 Alicante, Spain; pascual_eli@gva.es

Accepted 9 July 2007


See linked article, p1311

Abbreviations: EULAR, European League Against Rheumatism; GP, general practitioner; MSU, monosodium urate; RA, rheumatoid arthritis; SUA, serum uric acid

Keywords: gout; monosodium urate crystals; quality of care

The first 150 words of the full text of this article appear below.

Gout has been recognised since ancient times, and we currently have a deep understanding of its pathophysiology. The disease results from a deposit of monosodium urate (MSU) crystals in joint structures and in other, generally periarticular, sites in the form of tophi. High serum uric acid (SUA) is required for the formation of these crystals. The most characteristic features of gout are acute attacks of joint inflammation, which frequently occur at the first metatarsophalangeal joint, although their occurrence in other joints and in bursae is also very common. Oligoarticular, polyarticular, and more protracted and lingering forms of the disease occur, and if untreated or poorly managed, the disease can become very persistent and disabling. Fortunately, we now have highly effective drugs enabling us to deal with gouty joint inflammation and to prevent their recurrence.1 An unequivocal diagnosis can be obtained by identifying MSU crystals in joint fluid obtained either during . . . [Full text of this article]


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