Allopurinol for gout: consider the case for limited HLA-B*5801 screening

THE INCIDENCE AND PREVALENCE of gout is increasing throughout the world, and general practitioners often provide initial management with the use of urate-lowering medications such as allopurinol.¹ Allopurinol, a xanthine oxidase inhibitor, reduces the conversion of hypoxanthine and xanthine to uric acid, and it constitutes up to 98% of the urate-lowering medications prescribed in Australia.² However, allopurinol can rarely cause severe cutaneous adverse reactions (SCAR) and allopurinol hypersensitivity syndrome (AHS). Estimated risks of developing SCAR from allopurinol range from 1:250 to 1:1000, with mortality rates of up to 25%.^1,3,4 Given the potentially serious consequence from such a commonly prescribed long-term medication, we outline the rationale behind opportunistic HLA-B*5801 screening in patients with gout in high-risk groups prior to initiating allopurinol to reduce the incidence of SCAR and AHS.^5–7