GOUT

hereditary metabolic disorder that is characterized by recurrent acute attacks of severe inflammation in one or more of the joints of the extremities. Gout results from the deposition, in and about the joints, of salts of uric acid, which is present in marked excess throughout the body in persons with the disorder. Uric acid is the metabolic end-product of purines and normally is steadily excreted into the urine. The biochemical defect that leads to abnormal concentration of the substance in the body is not yet known. Although gout is probably inborn, the initial attack of acute joint inflammation, or gouty arthritis, usually does not appear until middle age. Any peripheral joint may be affected, but, for some reason, the joint at the base of the big toe is especially susceptible. Heat, redness of the skin, and extreme tenderness and pain of the affected joints are symptoms. An attack, even when untreated, may subside in a week or two. Attacks may come and go without apparent reason, but there are a number of precipitating factors, including acute infection, emotional upset, diuresis, surgery, trauma, and the administration of certain drugs. Precipitation of microscopic amounts of uric acid in the joint cartilage precedes the first attack. In some cases, continued deposition of uric acid salts may cause knobby deformities and may also occur in cartilage that is not associated with the joints, such as the rim of the ear. The classic treatment for an acute attack of gouty arthritis is the administration of colchicine. More recent medications include allopurinol (4-hydroxypyrazalopyrimidine) and related compounds, which inhibit the synthesis of uric acid in the body. Gout is one of the oldest diseases in medical literature, as colchicine is one of the oldest drugs in therapeutics. Nor is the condition uncommon; it accounts for at least 5 percent of all significant problems in the field of systemic arthritis. It is uncommon, however, in women; the male-female ratio is 20:1.