Clinical Information

Uric acid is the final product of purine metabolism in humans. Purines, compounds that are vital components of nucleic acids and coenzymes, may be synthesized in the body or they may be obtained by ingesting foods rich in nucleic material (eg, liver, sweetbreads). Approximately 75% of the uric acid excreted is lost in the urine; most of the remainder is secreted into the gastrointestinal tract, where it is degraded to allantoin and other compounds by bacterial enzymes.

Asymptomatic hyperuricemia is frequently detected through biochemical screening. The major causes of hyperuricemia are increased purine synthesis, inherited metabolic disorder, excess dietary purine intake, increased nucleic acid turnover, malignancy, cytotoxic drugs, and decreased excretion due to chronic renal failure or increased renal reabsorption. Long-term follow-up of these patients is undertaken because many are at risk of developing renal disease; few of these patients ever develop the clinical syndrome of gout.

Hypouricemia, often defined as serum urate <2.0 mg/dL, is much less common than hyperuricemia. It may be secondary to severe hepatocellular disease with reduced purine synthesis, defective renal tubular reabsorption, overtreatment of hyperuricemia with allopurinol, as well as some cancer therapies (eg, 6-mercaptopurine).