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Mechanism  compete with uric acid in PCT  increase uric acid
excretion.

 Used in chronically. No value in acute attacks.

Toxicity

 Uricosuric agents (weak acids) also inhibit the secretion of other
weak acids like penicillin and methotrexate.

 Hypersensitivity because they are sulphonamides share
allergenicity with other sulphonamides

Xanthine oxidase inhibitors

Mechanism  inhibit enzyme xanthine oxidase (the enzyme that

metabolize conversion of hypoxanthine into xanthine and xanthine into
uric acid)  result decrease production of Uric acid

 Allopurinol  converted into alloxanthine  inhibit enzyme

irreversibly

 Fubuxostat  reversible inhibitor (more effective drug) (non-
purine inhibitor of xanthine oxidase)

Uses

 Chronic gout treatment

 In combination with colchicine or NSAIDs in acute attacks

 Adjunctive in treatment of cancer therapy  slow the formation of
uric acid from purines by death of neoplastic cells.

Toxicity

 GIT upset + rash + peripheral neuritis + bone marrow dysfunction +
aplastic anemia

Contents

Pharmacology Mnemonics and Short Notes By Muhammad Ramzan Ul Rehman