ALLOSIG

What it is

ALLOSIG contains allopurinol, available as 100 mg and 300 mg tablets. Allopurinol inhibits xanthine oxidase, the enzyme which catalyses the conversion of hypoxanthine to xanthine, and of xanthine to urate/uric acid, thereby decreasing urate formation.

Approved indications

— Gouty arthritis, skin tophi and/or renal involvement through crystal deposition or stone formation resulting from main clinical manifestations of urate/uric acid deposition — Idiopathic gout — Uric acid lithiasis — Acute uric acid nephropathy — Neoplastic disease and myeloproliferative disease with high cell turnover rates — Enzyme disorders including hypoxanthine guanine phosphoribosyltransferase (including Lesch-Nyhan syndrome), glucose-6-phosphatase (including glycogen storage disease), phosphoribosylpyrophosphate synthetase, and phosphoribosylpyrophosphate amidotransferase — Management of 2,8-dihydroxyadenine (2,8-DHA) renal stones related to deficient activity of adenine phosphoribosyl transferase — Management of recurrent mixed calcium oxalate renal stones in the presence of hyperuricosuria, when fluid, dietary and similar measures have failed

Dosing overview

ALLOSIG may be taken orally once a day after a meal and is well tolerated, especially after food. For adults, dosing ranges from 100 to 200 mg daily in mild conditions, 300 to 600 mg daily in moderately severe conditions, or 700 to 900 mg daily in severe conditions. The dosage should be adjusted by monitoring serum urate concentrations and urinary urate/uric acid levels at appropriate intervals.

Key safety warnings

ALLOSIG should be discontinued at the first appearance of skin rash or other signs which may indicate an allergic reaction, as a skin rash may be followed by more severe hypersensitivity reactions such as exfoliative, urticarial, and purpuric lesions as well as Stevens-Johnson syndrome (SJS), drug rash with eosinophilia and systemic symptoms (DRESS), Lyell's syndrome, generalised vasculitis, irreversible hepatotoxicity, and on rare occasions death. The HLA-B*5801 allele has been shown to be associated with the risk of developing allopurinol-related hypersensitivity syndrome and SJS/TEN, with frequency up to 20% in Han Chinese population, 8–15% in Thai population, about 12% in Korean population and 1–2% in individuals of Japanese or European origin, and screening for HLA-B*5801 should be considered before starting treatment in patient subgroups where the prevalence of this allele is known to be high. ALLOSIG treatment should not be started until an acute attack of gout has completely subsided, as further attacks may be precipitated, and in the early stages of treatment an acute attack of gouty arthritis may be precipitated, therefore prophylaxis with a suitable anti-inflammatory agent or colchicine (0.5 mg three times a day) for at least one month is advisable. Bone marrow depression has been reported in patients receiving allopurinol, most of whom received concomitant medicines with the potential for causing this reaction, occurring as early as six weeks to as long as six years after the initiation of therapy, and rarely a patient may develop varying degrees of bone marrow depression while receiving allopurinol alone.

Contraindications

ALLOSIG should not be administered in individuals known to be hypersensitive to allopurinol or to any other ingredients of the product. ALLOSIG should not be given concomitantly with iron salts to patients with idiopathic haemochromatosis, nor should it be given to the immediate relatives of such patients. ALLOSIG is contraindicated in children with the exception of those with hyperuricemia secondary to malignancy or with Lesch-Nyhan syndrome.

Regulatory history

ALLOSIG allopurinol tablets (100 mg and 300 mg) were first listed on the Australian Register of Therapeutic Goods on 22 February 2017.