Interleukin-1β (IL-1β) is a key mediator of the inflammatory response. Because of this, IL-1β inhibitors are being used to combat inflammation in many common conditions, such as gout. However, although IL-1β inhibitors have been shown to shorten gout attacks, it is unclear if they can prevent gout attacks altogether. In a study recently published in Annals of Internal Medicine, researchers examine the relationship among canakinumab, a monoclonal antibody targeting IL-1β; serum uric acid levels; and the incidence of gout attacks.
— Annals of Int Med (@AnnalsofIM) September 19, 2018
Of interest: IL-1beta blockade with quarterly canakinumab administration was associated with significantly reduced risk for gout attacks without any change in serum uric acid levels. https://t.co/T0WgcjSmD3
— Thomas Dayspring (@Drlipid) September 17, 2018
In a secondary exploratory analysis of a randomized controlled trial, clinical sites in 39 countries were used to collect participants. For the analysis, 10,059 patients with a prior myocardial infarction and a high-sensitivity C-reactive protein (hsCRP) level of at least 19.1 nmol/L were used.
— GoutandYou (@GoutandYou) September 19, 2018
— Annals of Int Med (@AnnalsofIM) September 18, 2018
Canakinumab (50 mg, 150 mg, or 300 mg) versus placebo was provided randomly, administered subcutaneously every 3 months. Then, the rates of gout attacks were compared across patients with different baseline concentrations of serum uric acid (≤404.5 µmol/L, 404.6 to 535.3 µmol/L, and ≥535.4 µmol/L) and in different intervention groups in Cox proportional hazards regression models.
Interleukin-1β Blockade, Incident Gout, and Serum Uric Acid Levels | Ann Intern Med | ACP | https://t.co/D8MkjaEl5I
— Daniel H Solomon (@DanielHSolomon) September 18, 2018
— Christos Koutsianas (@Dr_C_Koutsianas) September 18, 2018
Results showed that canakinumab did not affect serum uric acid levels over time yet significantly reduced rates of gout attacks at all baseline concentrations of serum uric acid. “These data have relevance for the development of agents for gout that target the IL-1β pathway of innate immunity,” the researchers concluded.
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SOURCE: Annals of Internal Medicine