Systemic effects of gout flares beyond the joints

Purpose of review

A gout flare is an episode of intense inflammation caused by the activation of NLR family pyrin domain containing 3 (NLRP3) inflammasome and production of interleukin (IL)-1β. This pathway is involved in pathogenesis of cardiovascular events and provides a plausible mechanism linking gout flares to cardiovascular diseases.

Recent findings

Gout flares are associated with a transient increased risk of cardiovascular events (myocardial infarction, stroke, and cardiovascular death), venous thromboembolism, and tachyarrhythmia in the subsequent 30–60  days – a finding comparable to that observed after other acute inflammatory states, such as influenza and pneumonia.

Treat-to-target urate-lowering therapy lowered the risk of major adverse cardiovascular events in an emulated target trial. It also reduced systemic inflammation in observational studies. Additionally, gout flare prophylaxis with colchicine was associated with lower rates of major adverse cardiovascular events in a nationwide cohort study without evidence of residual confounding.

Summary

Patients with gout are at a high risk of cardiovascular diseases. Recent data suggest that patients presenting with gout flares warrant heightened vigilance for cardiovascular events, venous thromboembolism, and tachyarrhythmia over the following 30–60 days. Treating gout to the target serum urate level could prevent cardiovascular events and renal function decline. Gout flare prophylaxis with colchicine may have a similar effect.