The diagnosis, pathophysiology, and treatment of gout

Abstract

Gout is the best known crystal-induced joint disorder. This disease, which is caused by monosodium urate crystal deposition occurs most commonly in men with a peak incidence in the fifth decade. Women also often get gout after menopause. Although gout is a result of hyperuricemia, asymptomatic hyperuricemia in the absence of gout is not a disease state. The typical initial attack of gout usually occurs in a single joint, often in the big toe. Without treatment gout evolves over years to chronic tophaceous gout often with chronic arthritis in up to 75% of cases. Detection of monosodium urate crystals is considered mandatory for establishing the diagnosis of gout as serum uric acid levels can be misleading. Coating of the crystals by different proteins may modify their inflammatory potential and may be an important modulating mechanism. Some portion of gouty inflammation after urate crystal deposition can result from binding of iron to crystals, which also augments neutrophil activity in vitro. For the appropriate treatment of acute gouty arthritis in the patients with multiple medical problems that may contraindicate nonsteroidal anti-inflammatory drugs or colchicine, the use of adrenocorticotropic hormone and triamcinolone acetonide can be considered. The use of cyclosporine in transplant surgery has created a whole new class of patients with gout that is difficult to manage. Patients taking cyclosporine often develop hyperuricemia and an early, polyarticular and tophaceous gout. Allopurinol can be used with adjustment of doses of any azathioprine that is being used. Benzbromarone also appears to be a promising drug in the cyclosporine treated renal transplant recipients, if they have a creatinine clearance over 25 mL per minute.