Abstract
IntroductionGout is a common arthritis that occurs particularly in patients who frequently have associated comorbidities that limit the use of conventional therapies. The main mechanism of crystal-induced inflammation is interleukin-1 production by activation of the inflammasome. We aimed to evaluate the efficacy and tolerance of anakinra in gouty patients.MethodsWe conducted a multicenter retrospective review of patients receiving anakinra for gouty arthritis. We reviewed the response to treatment, adverse events and relapses.ResultsWe examined data for 40 gouty patients (32 men; mean age 60.0 ± 13.9 years) receiving anakinra. Mean disease duration was 8.7 ± 8.7 years. All patients showed contraindications to and/or failure of at least two conventional therapies. Most (36; 90%) demonstrated good response to anakinra. Median pain on a 100-mm visual analog scale was rapidly decreased (73.5 (70.0 to 80.0) to 25.0 (20.0 to 32.5) mm, P <0.0001), as was median C-reactive protein (CRP) level (130.5 (55.8 to 238.8) to 16.0 (5.0 to 29.5) mg/l, P <0.0001). After a median follow-up of 7.0 (2.0 to 13.0) months, relapse occurred in 13 patients after a median delay of 15.0 (10.0 to 70.0) days. Seven infectious events, mainly with long-term use of anakinra, were noted.ConclusionsAnakinra may be efficient in gouty arthritis, is relatively well tolerated with short-term use, and could be a relevant option in managing gouty arthritis when conventional therapies are ineffective or contraindicated. Its long-term use could be limited by infectious complications.
Highlights
Gout is a common arthritis that occurs in patients who frequently have associated comorbidities that limit the use of conventional therapies
Gout is a common arthritis caused by deposition of monosodium urate (MSU) crystals within and around joints secondary to chronic hyperuricemia
Only two small open studies have evaluated the efficacy of anakinra in acute gouty arthritis [13,14] anakinra has been labeled for rheumatoid arthritis treatment for more than 10 years
Summary
Gout is a common arthritis that occurs in patients who frequently have associated comorbidities that limit the use of conventional therapies. The main mechanism of crystal-induced inflammation is interleukin-1 production by activation of the inflammasome. Gout is a common arthritis caused by deposition of monosodium urate (MSU) crystals within and around joints secondary to chronic hyperuricemia. It affects 1% to 2% of adults in developed countries and may be increasing in prevalence [1]. The main mechanism of crystal-induced inflammation is interleukin 1b (IL-1b) production by activation of the NLRP3 inflammasome [8], which strengthens the relevance of targeting IL-1b in patients with crystal-induced arthritis. Anti-IL-1 agents, such as anakinra, have been evaluated in gouty arthritis, for treating acute attacks or for preventing gouty attacks while initiating urate-lowering therapy [9,10,11,12,13,14]. Other IL-1 inhibitors, canakinumab and rilonacept, appear to be effective in reducing pain and signs of inflammation in randomized controlled trials, which validate IL-1 as playing a pivotal role in gout inflammation [9,10,12,15]
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