Tissue concentrations of allopurinol have not been reported in humans, but it is likely that allopurinol and oxipurinol will be present in the highest concentrations in the liver and intestinal mucosa where xanthine oxidase activity is high.The main metabolite of Allopurinol tablets is oxipurinol. Posology. cyclophosphamide, doxorubicin, bleomycin, procarbazine, alkyl halogenides), blood dyscrasias occur more frequently than when these active substances are administered alone.
The apparent volume of distribution of allopurinol is approximately 1.6 litre/kg which suggests relatively extensive uptake by tissues. After recovery from mild reactions, Allopurinol tablets may, if desired, be re-introduced at a small dose (e.g. In addition to the inhibition of purine catabolism in some but not all hyperuricaemic patients, de novo purine biosynthesis is depressed via feedback inhibition of hypoxanthine-guanine phosphoribosyltransferase. Initially 100 mg daily, taken preferably after food; dose to be increased according to response, up to 900 mg daily in divided doses (max. Elimination of allopurinol is mainly by metabolic conversion to oxipurinol by xanthine oxidase and aldehyde oxidase, with less than 10% of the unchanged drug excreted in the urine. Rechallenge should not be undertaken in patients with hypersensitivity syndrome and SJS/TEN. If the rash recurs, Allopurinol tablets should be permanently withdrawn as more severe hypersensitivity may occur (see Immune system disorders). This information is intended for use by health professionalsWhite to off white, round, biconvex, uncoated tablet with inscription "AW" on one side and plain on the other sideAllopurinol is indicated for reducing urate/uric acid formation in conditions where urate/uric acid deposition has already occurred (e.g. The highest risk for SJS and TEN, or other serious hypersensitivity reactions, is within the first weeks of treatment. 10–20 mg/kg daily, dose to be taken preferably after food; maximum 400 mg per day. Reported values for the elimination half-life range from 13.6 hours to 29 hours. Blood count monitoring should therefore be performed at regular intervals. It appears to be reversible on withdrawal of Allopurinol tablets.4 In early clinical studies, nausea and vomiting were reported. 50 mg/day) and gradually increased. Peak plasma levels of allopurinol generally occur approximately 1.5 hours after oral administration of Allopurinol, but fall rapidly and are barely detectable after 6 hours. Allopurinol has a plasma half-life of about 1 to 2 hours.Oxipurinol is a less potent inhibitor of xanthine oxidase than allopurinol, but the plasma half-life of oxipurinol is far more prolonged. The main clinical conditions where urate/uric acid deposition may occur are: idiopathic gout; uric acid lithiasis; acute uric acid nephropathy; neoplastic disease and myeloproliferative disease with high cell turnover rates, in which high urate levels occur either spontaneously, or after cytotoxic therapy; certain enzyme disorders which lead to overproduction of urate, for example: hypoxanthine-guanine phosphoribosyltransferase, including Lesch-Nyhan syndrome; glucose-6-phosphatase including glycogen storage disease; phosphoribosylpyrophosphate synthetase, phosphoribosylpyrophosphate amidotransferase; adenine phosphoribosyltransferase. Adequate hydration to maintain optimum diuresis facilitates excretion of allopurinol and its metabolites. You'll have regular blood tests to monitor your uric acid levels.

If you require BNF, use 10–20 mg/kg daily, dose to be taken preferably after food; maximum 400 mg per day.Initially 100 mg daily, taken preferably after food; dose to be increased according to response, up to 900 mg daily in divided doses (max.