How interleukin‐1β induces gouty arthritis

Recent clinical trials with IL-1β blockade have revealed an impressive and sustained reduction in recurrent attacks of gouty arthritis (1).Even with the use of allopurinol to reduce the systemic levels of uric acid and the anti-inflammatory properties of colchicine, there is no dearth of patients with recurrent episodes of painful gouty arthritis poorly controlled with these regimens who require intermittent courses of glucocorticoids.Thus, the success of IL-1β blocking therapies is a welcome addition for treating refractory gouty arthritis in these patients.Despite the availability of several widely used TNFα blocking therapies for rheumatoid arthritis and other autoimmune diseases, there is a paucity of reports that blocking TNFα provides an effective reduction in gout severity.One explanation for the lack of clinical trials of TNFα blockade in gout attacks is reluctance of subjecting these patients to suppression of host-defense by TNFα blockers.An alternative explanation is that efficacy of TNFα blockade in refractory gout is less than expected.One study reports a weak response with rather high doses of infliximab (2).There are also few publications on monosodium urate (MSU) crystals inducing TNFα from human and mouse cells unless co-stimulated with endotoxins.Therefore, IL-1β blockade may be used for inducing long-term remissions in refractory patients and replace glucocorticoids.If IL-1β blockade becomes the standard of care in refractory gout, it would be consistent with the unique role of IL-1β in the pathogenesis of auto-inflammatory diseases.