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Gout is a common arthritis caused by deposition of monosodium urate (MSU) crystals in joints after long-standing hyperuricaemia. Patients with gout often have comorbidities such as cardiovascular (CV) disease, renal failure and metabolic syndrome components. About two-thirds have hypertension, half are obese and half have diabetes. Prospective and interventional studies have demonstrated that hyperuricaemia and gout are associated with increased risk of myocardial infarction (MI) and death primarily because of increased risk of CV events.1 Thus, knowledge of the effects of allopurinol, the most frequently used urate-lowering therapy, on risk of MI is of prime importance.
In this context, the report from de Abajo and colleagues2 is of interest: this population-based case-control study found that allopurinol was associated with significantly reduced risk of non-fatal acute MI (OR=0.52 (95% CI 0.33 to 0.83)), mainly in men, with >180 days’ allopurinol exposure and with >300 mg dose.
These exciting findings raise several issues: how does allopurinol decrease the risk of MI? Is it through xanthine oxidase (XO) inhibition and/or through a decrease in urate levels?
Hyperuricaemia, gout and CV events
The mechanisms linking hyperuricaemia and gout with CV events are not yet completely revealed but may include oxidative stress generated by XO, the enzyme that catalyses the formation of urate (figure 1). Other mechanisms are a direct …
Competing interests PR received fees from Ménarini, Ipsen, Savient and Astra Zeneca.
Provenance and peer review Commissioned; internally peer reviewed.
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