Abstract

Contrary to the general assumption that gout is a benign condition, epidemiologic studies have demonstrated gout to be associated with increased risk of cardiovascular events and all causes of mortality1. From a social viewpoint, gout also has a substantial effect on work, resulting in work absence and decreased productivity2. Moreover, in some patients, it can lead to severely impaired quality of life. For example, scores of the Medical Outcomes Survey Short-Form 36 (SF-36) for patients with gout were found comparable to those of patients with severe, debilitating rheumatoid arthritis3. Also, Becker, et al found that subjects with treatment-failure gout had mean SF-36 scores that were analogous to those of healthy individuals aged 75 years and older4. Progression of gout from solely acute flares to severe chronic disease, characterized by palpable tophi combined with urate crystal arthropathy, is most often the result of failure of urate-lowering therapy (ULT) to reach the target of 6 mg/dl to achieve crystal dissolution, and/or poor adherence of patients to ULT5. This failure to lower serum uric acid (sUA) levels below the European recommended cutoff of 6 mg/dl (360 μM)6 or the British recommended cutoff of 5 mg/dl (300 μM)7 usually occurs in patients intolerant to, or whose disease is refractory to, currently available ULT agents. This is the case with allopurinol in particular because of the frequency of allergic reactions or when medical comorbidities, mainly renal failure, limit the extent of its use. In organ transplant recipients, for whom therapy to prevent graft rejection includes azathioprine, use of xanthine oxidase … Address correspondence to Prof. P. Richette, Fédération de Rhumatologie, Hôpital Lariboisière, 2 Rue Ambroise Paré, 75475 Paris cedex 10, France. E-mail: pascal.richette{at}lrb.aphp.fr

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