Purine ribonucleotides are degraded to uric acid by a complexly regulated metabolic pathway. Abrupt lowering of intracellular ATP, a physiological inhibitor of this pathway at normal concentrations, precipitates a cascade of nucleotide catabolism. The clinical syndrome of accelerated purine ribonucleotides catabolism, as defined by hyperuricemia, hyperuricosuria and elevated urinary oxypurines, has primary and secondary causes. Treatment of these disorders is in general directed toward reversal of the precipitating factors, inhibition of further nucleotide degradation, and stimulation of purine nucleotide and ATP formation. Careful clinical application of these principles seems indicated.