A STUDY OF THE HYPERURICEMIA INDUCED BY HYDROCHLOROTHIAZIDE AND ACETAZOLAMIDE SEPARATELY AND IN COMBINATION*

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Abstract
A study of the hyper-uricemic effect of acetazolamide and hydrochlorothiazide in humans revealed that acetazolamide produced a modest hyperuricemia and a decreased urinary excretion of uric acid and, when given with hydrochlorothiazide, potentiated the hyperuricemic effects of the latter drug. The hyperuricemia produced by hydrochlorothiazide was associated with an increased urinary excretion of uric acid when doses of 75 mg or less were used each day and with a decreased excretion of uric acid when larger doses were used. An explanation of the dual effect of hydrochlorothiazide is suggested by the known ability of EATDA (2-ethylamino-l,3,4-thiadiazole) to produce uricogenesis in man. EATDA is closely related to acetazolamide (2-acetylamino-l,3,4-thiadiazole-5-sulfonamide) differing mainly in its lack of a sulfonamide group. The sulfonamide containing diuretic drugs may produce hyperuricemia by a complex metabolic effect on nucleic acid degradation and purine nucleotide synthesis and the final production of excretion of uric acid is dependent upon how effectively the sulfonamide containing drug inhibits the compensatory synthesis of purine nucleotides.