It competitively inhibits xanthine oxidase, so prevents further uric acid synthesis |
It catalyzes the oxidation of already synthetized uric acid into allantoin |
It does not directly alter acid uric levels, so its action is slower and gradual, within 24 - 48 h and reaches a maximum after 7-10 days |
Its action is faster in controlling uricemia, within 4 h |
It may increase creatinine levels |
It may reduce creatinine levels and urea nitrogen, by improving renal function |
It increases precursors of uric acid, such as xanthine, less soluble in urine than uric acid. It may impair renal function and improve stone formation. |
It does not require alkalinization, so calcium phosphate's stones formation is less probable. |
Its formulation is oral since 1966. Since 1999 a new intravenous formulation (not yet available in Italy) was introduced in USA |
An intravenous formulation is available |
It needs an adjustment of doses if patient has renal impairment, because its active metabolite, oxypurinol, is excreted in urine. |
No adjustment of doses is necessary if patient has renal or hepatic impairment. In renal failure, allantoin may accumulate, but it is not toxic. |
It has drug-drug interaction with very common agents (chlorpropamide, 6-mercaptopurine, azathioprine, dicumarol, cyclosporine, thiazide diuretics) |
No drugs interactions are referred |