ALLOPURINOL AND STEVENS-JOHNSON RISK

Dr Foong helpfully highlights the well-established rare link between allopurinol and Stevens-Johnson syndrome, by reviewing the results of the EuroSCAR study (HBB Foong. Allopurinol and the risk of Stevens-Johnson syndrome and toxic epidermal necrolysis. J R Coll Physicians Edinb 2009; 39:144–5). At rates of two per million population, it remains an extremely unusual phenomenon. His conclusions that ‘more often than not the drug is prescribed for asymptomatic hyperuricaemia’ are erroneous and lack evidence. The retrospective report of eight patients from 23 years ago and literature review which he quotes clearly do not provide a clear enough sample size to form a judgement.

Hypersensitivity of a more benign nature is frequently mentioned as a reason for discontinuing allopurinol. However, it is estimated that 95% of patients are able to tolerate allopurinol.¹ Side effects can include rash, diarrhoea, leukopenia, pruritis and fever. If the manifestations are only cutaneous, then desensitisation can be attempted commencing at doses as low as 50 μg and increasing to 100 mg over a four-week period. More than 70% of such patients are able to continue to take allopurinol, although sometimes late adjustment of the dose may be required. Education for practitioners regarding desensitisation regimens should allow more patients to tolerate the drug. Gout is undertreated at present, and patients should be on doses of allopurinol that allow a serum urate of <0.36 mmol/l.^2,3 Dose titration can escalate to 900 mg if required. Undertreatment leads to flare and tophaceous disease, with radiographic damage and disability.⁴

Adverse reactions with allopurinol are unfortunate but extremely rare and should not be used as a reason for lowering the appropriate dosage of allopurinol as agreed in both national and international guidelines.2,3