New England Journal of Medicine · 1969 · 168 citations · 6 references
MedicinePharmacologyPharmacotherapyRenal PharmacotherapyUrolithiasisUrologic OncologyGoutGout PharmacotherapyPharmacologic Management Of GoutStone PathogenesisUric Acid StonesNeoplastic DiseaseUric Acid MetabolismUric Acid Stone Formation
SINCE its clinical introduction in 1964, allopurinol (4-hydroxypyrazolo-[3,4-d]-pyrimidine) has been increasingly used for the treatment of hyperuricemia of gout,1 , 2 many neoplastic diseases and other metabolic disorders. Allopurinol and its principal metabolic product, oxipurinol (alloxanthine, oxoallopurinol), inhibit the enzyme, xanthine oxidase, that normally converts hypoxanthine to xanthine, and xanthine to uric acid. The concentration of these oxypurine precursors of uric acid in blood and urine thus increases in patients treated with allopurinol.Although the formation of urinary xanthine stones has been anticipated as a possible complication of allopurinol therapy, to date this occurrence has not been documented in the clinical use . . .
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