We now have sufficient knowledge to be able to identify the factors contributing to hyperuricemia in most patients with gout. Some of these factors, such as obesity, a high-purine diet, regular alcohol consumption, and diuretic therapy, may be correctable. In patients with persistent hyperuricemia, regular medication should lower the serum urate concentration to an optimal level. The continuing challenge is to educate patients about correctable factors and the importance of regular medication and ensure their compliance so that attacks of gout do not recur.

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The oral or intravenous administration of fructose to children results in dramatic rises in both urate and lactate concentrations in serum and an increase in the excretion of uric acid in the urine, findings interpreted as being caused by rapid nucleic acid degradation due to the increased intracellular lactic acidosis in the liver (Perheentupa and Raivio, 1967). As lactate also reduces renal excretion of urate (Yu, Sirota, Halpern, and Gutman, 1967), these authors were unable to assess the relative importance of hepatic and renal factors in the resultant hyperuricaemia, but the increase in the urinary uric acid suggested either a sudden increase in urate production or a shift of urate from an intracellular pool to the extracellular fluid. Moreover, Fox and Kelley (1972) were unable to demonstrate any consistent decrease in the fractional clearance of urate after fructose infusions. Studies in Cebus monkeys have also demonstrated hyperuricaemia and increases in urinary uric acid excretion after infusions of high concentrations of hexoses, fructose having the greatest effect and glucose a lesser effect (Simkin, 1969). This has not been a uniform finding, however, and no significant changes in serum urate concentrations were demonstrated during the 3 hrs after the intravenous administration of 100 g. fructose to ten young adult males (Curreri and Pruitt, 1970). Because of the conflicting evidence, the lack of information concerning the possible mechanism involved and the potential importance in patients with hyperuricaemia, it was decided to compare the effect of diets containing large quantities of either added fructose or glucose on urate metabolism, as reflected by the miscible urate pool and turnover rate and the simultaneous incorporation of glycine into both urinary and produced uric acid. Methods SUBJECTSThe three patients studied were males who were healthy apart from stable chronic neurological disease. Each was studied on three occasions, and each study was separated by at least 4 months, which allowed complete elimination of isotopes used in the previous study. None had suffered from gout; all had normal serum urate concentrations and only Subject A had suffered from any renal disease, which in his case had consisted of occasional urinary tract infections responding readily to chemotherapy. All understood the implications of the study and were fully agreeable and cooperative. All studies were carried out in hospital under metabolic ward conditions. DIET Purine-free diets containing sufficient calories to maintain a stable weight were used throughout. Each diet was begun at least 5 days before isotope administration and was continued for the 7 study days, during which all urine was collected. Fluids were taken regularly during the day and intake was as large as was desired by the patient but at least sufficient to maintain a urine volume in excess of 1 litre per 24 hrs.Three dietary regimes were used (Table). The first study in each subject had been completed before the planning of the glucose and fruc...