Article Text

AB1080 Effect of serum urate level on prevention of flare in acute gouty arthritis patients with canakinumab
  1. P. Sunkureddi1,
  2. N. Schlesinger2,
  3. T. Kiechle3,
  4. A. Shpilsky4,
  5. A. So5
  1. 1Clear Lake Rheumatology Center, Texas
  2. 2Umdnj-Rwjms, New Jersey, United States
  3. 3Novartis Pharma AG, Basel, Switzerland
  4. 4Novartis Pharmaceuticals Corporation, East Hanover NJ, United States
  5. 5CHUV, University of Lausanne, Lausanne, Switzerland


Background Lowering serum urate (SU) level is considered to be the mainstay of gouty arthritis (GA) therapy. SU levels below 6mg/dL favor dissociation of monosodium urate deposits (microtophi and visible tophi) in the joints and therefore these patients are less likely to flare.

Objectives To explore the impact of baseline SU level on the occurrence of new flares in patients treated for acute GA with anti-inflammatory therapy.

Methods A retrospective exploratory analysis using a multivariate logistic regression model predicting new flare was performed using the pooled data of 454 patients from two, pivotal 12-week, multicenter, double-blind, double dummy, active-controlled studies (β-RELIEVED and β-RELIEVED II). In these two studies, GA patients (meeting preliminary ACR-1977 criteria) with flare duration ≤5 days and contraindicated, intolerant or unresponsive to NSAIDs and/or colchicine were randomized to receive a single dose of canakinumab 150mg sc or triamcinolone acetonide (TA) 40mg im and were re-dosed “on demand” on each new flare. Patient’s baseline characteristics deemed to be indicative of GA disease severity were prescreened using a likelihood ratio test in a series of logistic regression models with treatment and a single covariate candidate.

Results In a single predictor model, SU level was not found to be a statistically significant (p=0.21) predictor of new flare, while number of tophi locations, frequency of flares, and number of joints (>1) affected by acute GA flare were found highly significant predictors of new flare (p<0.05) in both the single predictor models and multivariate analysis. When added to the severity adjusted multivariate model, SU level appears to be a noise variable (p=0.50) compared to the triplet of the strongest determinants of reflare.

Conclusions Results of this retrospective exploratory analysis show that baseline SU level was not a predictor of new flares in patients receiving anti-inflammatory therapy for acute GA, suggesting that GA severity may be more closely related to the prevention of flare than the baseline SU level.

Disclosure of Interest P. Sunkureddi Consultant for: Novartis, Bristol Myers Squibb, UCB, Pfizer., Speakers Bureau: Novartis, Bristol Myers Squibb, UCB, Pfizer., N. Schlesinger Grant/Research support from: Novartis, Consultant for: Novartis, URL Pharma, Savient, Takeda, Rx Enzyme, Speakers Bureau: Novartis, Takeda, Savient, T. Kiechle Shareholder of: Novartis, Employee of: Novartis, A. Shpilsky Shareholder of: Novartis, Employee of: Novartis, A. So Grant/Research support from: Novartis, Consultant for: Novartis, Ardea, Speakers Bureau: Novartis, Ardea, Menarini

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