Abstract
I thank Dr Perry for his interest in my article. I agree with him that if the manifestations of the side effects of allopurinol are mild, then desensitisation can be attempted at a lower dose. However, isolated asymptomatic hyperuricaemia does not warrant the use of allopurinol. One must distinguish the difference between gout and hyperuricaemia. Dr Perry’s references on the rheumatology guidelines for the management of gout apply to cases of gout and not to hyperuricaemia.1 In fact, the indications for allopurinol therapy are tophaceous gout, major uric acid overproduction (proven by urinary excretion >53 mmol/24 hours) frequent gouty attacks, recurrent uric acid renal calculi and prevention of acute urate nephropathy in patient receiving cytotoxic therapy for malignancies.2
In a study by Khoo3 a total of 13 patients were admitted for severe cutaneous adverse reactions to allopurinol during a three-year period. Almost 92% of them suffered from allopurinol hypersensitivity reactions, which included four patients with Stevens-Johnson syndrome. Allopurinol hypersensitivity syndrome, in contrast to other purely cutaneous drug eruptions, deserves special attention because of its multi-organ involvement, the liver and kidneys being most commonly affected. It was interesting to note that none of the 13 patients had clear clinical indications for allopurinol therapy. Asymptomatic hyperuricaemia is not uncommon, affecting an estimate of 5–8% of the population. As the risks, morbidity and mortality outweigh the benefits, it should only be prescribed when it is truly indicated.
Get full access to this article
View all access options for this article.
