gout, condition that manifests itself as recurrent attacks of acute arthritis, which may become chronic and deforming. It results from deposits of uric acid crystals in connective tissue or joints. The presence of increased uric acid (a breakdown product of DNA) in the body distinguishes gout from other forms of arthritis, although hyperuricemia alone, which often occurs in the complete absence of gout, is not thought to be the sole causative factor. About 95% of patients with this disorder are men, usually over 30. Gout is associated with obesity and a hereditary factor in some cases. Diet also has an affect on gout. Consumption of meat and seafood, which are high in purine (from which digestion produces uric acid), increase the risk of gout, and gout is worsened by kidney problems and drinking alcoholic beverages, which slow the excretion of uric acid. Beer, which is higher than other alcoholic beverages in purines, also has been shown to increase the risk of gout.
Gout usually begins with an acute attack of pain, inflammation, extreme tenderness, and redness in the affected joint—often the big toe and sometimes the ankle or knee. After repeated attacks the disease can cause the deposition of sodium urate crystals in the tissues about the joints, causing stiffness and deformity. The aim of treatment is to minimize the formation of uric acid crystals. A high liquid intake that increases daily urine output is usually recommended. An acute attack of gout is usually treated with nonsteroidal anti-inflammatory drugs, such as indomethecine or naproxen, or the corticosteroid prednisone. Colchicine, a preparation of the meadow saffron, used since 1763 for gout, is still used when symptoms are not controlled by other drugs. Allopurinol and other xanthine oxidase inhibitors are used to prevent gout attacks in patients with chronically elevated uric acid levels; they lower uric acid concentrations in the blood by inhibiting the conversion of xanthine to uric acid.