Why is gout so poorly managed?

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Abstract
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 the attacks2 or at intercritical periods from previously inflamed asymptomatic joints of untreated subjects,3 4 or from a tophus. This procedure requires only skill in performing arthrocentesis and familiarity with the use of the polarised microscope, both a part of the core curriculum in rheumatology. The deposited crystals responsible for the disease dissolve when SUA levels are brought back to normal,3 5 and the time for total dissolution relates to the duration of the disease; after 1 year of adequate hypouricaemic treatment, crystals have usually disappeared from the joints if the disease duration has not been too long.6 In the absence of MSU crystals, attacks of gout are impossible, and the disease can be considered cured. Patients who have formed MSU crystals on one occasion appear to easily form them anew if SUA levels are allowed to rise again, prompting the return of the disease.7 8 To avoid this, lifelong hypouricaemic drug treatment is necessary after the crystals have dissolved, although for some patients dietary and lifestyle modifications may suffice. Finally, in an important proportion of patients with gout, hyperuricaemia is a part of metabolic syndrome and the presence of gout should make clinicians aware of associated morbidities, which are reversible, at least to some extent, by modifying dietary and lifestyle habits. The recent publication of guidelines on gout diagnosis9 and management10 by the European League Against Rheumatism (EULAR), the quality of care indicators from the US,11 and outcome measures for clinical trials12 outline the current interest in gout.

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