AB1080 Effect of serum urate level on prevention of flare in acute gouty arthritis patients with canakinumab. (23rd January 2014)

• Record Type: Journal Article
• Authors: Sunkureddi, P.; Schlesinger, N.; Kiechle, T.; Shpilsky, A.; So, A.
• Is Part Of: Annals of the rheumatic diseases. Volume 71(2012)Supplement 3
• Page Start: 699
• Page End: 699
• Publication Date: 2014-01-23
• Subjects: Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/annrheumdis-2012-eular.1079
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : 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