A drug which reduces the concentration of uric acid in the blood. It is used in the long term prevention of gout. Thank you to CentrX BioTech for inspiration.
Xanthine oxidase inhibitor
Prophylaxis of gout
Purines are essential components of DNA. The metabolic pathway of purines ends in uric acid which isn't very soluble in blood or urine. When uric acid precipitates out in the joints as monosodium urate crystals it causes gout.
The end of the metabolic pathway of purines:
Hypoxanthine +O2 + 2H2O xo⇒ Xanthine + 2H2O2
Xanthine + O2 + 2H2O xo⇒ Uric acid + 2H2O2
(xo⇒ - oxidation reaction catalysed by xanthine oxidase)
Allopurinol inhibits this pathway. Less uric acid ⇒ fewer crystals ⇒ less gout. (Hypoxanthine and xanthine are both more soluble than uric acid, and they can be excreted in the urine.) Allopurinol is exactly the same as hypoxanthine but with a Carbon and a Nitrogen swapped over.
First it acts as a competitive inhibitor of Xanthine Oxidase,
Allopurinol +O2 + 2H2O xo⇒ Alloxanthine (aka oxipurinol) + 2H2O2
Alloxanthine then binds irreversibly with Xanthine Oxidase, deactivating it.
Not to be started in acute gout, (but do continue treatment if an attack of acute gout occurs when already taking allopurinol.)
The initiation of Allopurinol can potentially trigger an attack of gout, so an NSAID or colchicine should be administered for about 3 months (until a month after blood levels of uric acid have been corrected.)
Among other things, Allopurinol interferes with the metabolism of azathioprine, theophylline, and anticoagulants. Doses of these drugs may need adjustment.
Gastrointestinal disorders. Rarely - Hypersensitivity reactions resembling Stevens-Johnson syndrome, withdraw therapy if a rash appears. Also rarely : vasculitis, hepatitis, malaise and headache.
Dosage for adults
100 mg orally daily after food, adjusted acording to uric acid concentration.
Date of most recent Update