Gout, one of the oldest recorded syndromes in medical history, is still a biochemical mystery. Primary gout is characterized by a derangement in purine metabolism and an elevated concentration of uric acid in the blood. Gout may also occur secondarily in diseases associated with reduced urinary excretion of uric acid or increased nuclear breakdown in body tissues. The metabolic abnormality in primary gout is probably an inherited trait, though this has not been proved.
The differential diagnosis of any swollen painful joint should always include gout. The most important diagnostic signs of gout are sudden periodic attacks of acute arthritis, an elevated level of serum uric acid, relief of pain by a therapeutic trial of colchicine and, later in the course of the disease, the presence of tophi around the joints or urate crystals in the synovial fluid. Renal damage is one of the major complications of chronic tophaceous gout and a frequent cause of death. Proteinuria is often the only manifestation of early renal involvement.
Treatment is discussed from the standpoints of diet, drug therapy, use of the artificial kidney, and the surgical excision of tophi. Described under drug therapy are the effects of colchicine (still the drug of choice for acute attacks), phenylbutazone, ACTH, corticosteroids, indomethacin, allopurinol, and the uricosuric agents (probenecid, salicylates and sulfinpyrazone).