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SAT0367 Low-Dose Anakinra is Effective for the Prophylaxis of Acute Episodes of Inflammation In Severe Tophaceous Gout.
  1. F. Perez-Ruiz1,
  2. A. M. Herrero-Beites2,
  3. A. Alonso-Ruiz1,
  4. J. Atxotegi1,
  5. M. R. Lopez-Santamaría1,
  6. M. de Miguel3
  1. 1Rheumatology Division. BioCruces Health Institute., HOSPITAL UNIVERSITARIO CRUCES, Baracaldo
  2. 2Rehabilitation Division, Hospital de Górliz. BioCRuces Helath Institute, Górliz
  3. 3Pharmacy Division, HOSPITAL UNIVERSITARIO CRUCES, Baracaldo, Spain


Background anakinra has been used off-label for the treatment of severe episodes of acute inflammation (EAIs) in gout [1], only a small retrospective series of 3 patients reported as prophylaxis with intermittent schedule [2].

Objectives to explore whether a low-dose prescription of anakinra would be useful in patients with severe gout and contraindication of other current treatments for prophylaxis of AEIs when starting urate-lowering therapy (ULT).

Methods patients with crystal proven arthritis, tophaceous gout, and severe, recurrent EAIs showing aformal contraindication for current treatments for prophylaxis and requiring repeated doses of parenteral corticosteroids were included in a cohort for follow-up. All patients were scheduled to start ULT and receive anakinra 100 mg sc once a week with additional 100 mg doses on demand during the first 3 months and only on demand dosing from month 3 to 6.

AEIs were evaluated using the EULAR-ACR preliminary criteria for self-referred AEIs in gout [3] and expressed as events/patient-year observation. Clinical evaluation and anaylsis (hemogram, full biochemistry including urate, estimated GF -CKD_EPI - and high sensitivity CRP) were monitored at baseline and months 3 and 6.

Results nine patients were included in the protocol, but 1 of them was excluded from analysis as he was shown to suffer also from crystal-proven chronic pyrophosphate inflammatory arthritis [4]. Mean age was 58±16 years (39-79), time with gout 9±4 years (5-16), polyarticular 75%. CHF was present in 4/8, CKD 3-4 in 6/8, serious AEs to NSAIDs in 6/8 and diabetes or steroid-induced hyperglycemia in 6/8.

Results are shown in Table. In the 0-3 period, only 2/8 required additional doses, and 4/8 while only on demand from mo 3-6. A patient had an episode of heart failure (4th in a year) but was maintained on treatment without further complications to date.

Conclusions this small sized pilot study is, to our knowledge, the first to explore in pre-established doses the efficacy of low-dose anakinra for the prophylaxis of AEIs in patients with severe comorbidities and severe tophaceous gout. These encouraging results deserve further studies.


  1. So A, DeSmedt T, Revaz S, Tschopp J. A pilot study of IL-1 inhibition by anakinra in acute gout. Arthritis Res Ther 2007;9:R28.

  2. Tran AP, Edelman J. Interleukin-1 inhibition by anakinra in refractory chronic tophaceous gout. Int J Rheum Dis 2011;14:e33-e37.

  3. Gaffo AL, Schumacher HR, Saag KG, Taylor WJ, Dinnella J, Outman R et al. Developing a provisional definition of a flare in patients with established gout. Arthritis Rheum 2012; 64: 1508-17.

  4. Zhang W, Doherty M, Bardin T, Barskova V, Guerne PA, Jansen TL et al. European League Against Rheumatism recommendations for calcium pyrophosphate deposition. Part I: terminology and diagnosis. Ann Rheum Dis 2011.

Disclosure of Interest F. Perez-Ruiz Consultant for: Ardea, Savient, Menarini, Astra, Metabolex, Pfizer, Novartis, SOBI, Speakers bureau: Menarini, A. Herrero-Beites: None Declared, A. Alonso-Ruiz: None Declared, J. Atxotegi: None Declared, M. Lopez-Santamaría: None Declared, M. de Miguel: None Declared

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