Session Type: Abstract Submissions (ACR)
Background/Purpose: Smoking has been identified as an important negative predictor of response to antirheumatic therapy. The aim of this study was to assess whether smoking status influenced the clinical response to rituximab (RTX) in an observational patient cohort with rheumatoid arthritis (RA).
Methods: Pooled data from the Collaborating European Registries for RTX in RA (CERERRA) project were used. Patients with RA who received at least 1 cycle with RTX and had at least 2 follow-up visits were included in the analyses. Smoking status was defined as smokers (current smokers) and non-smokers (never and ex-smokers). Baseline characteristics were compared by means of descriptive statistics. Analysis of co-variance (ANCOVA) was performed with DeltaDAS28 at 6 months as the dependent variable and smoking status as well as other baseline variables (age, sex, disease duration, number of prior biologic DMARDs) as covariates. Separate analyses were made for anti-CCP positive and negative patients.
Results: A total of 2431 patients with available smoking information were included – 1916 (79%) were non-smokers and 515 (21%) were smokers. 81% were female and 80% (out of 1199 patients with available anti-CCP status) were anti-CCP positive. Smokers had shorter disease duration than non-smokers (mean±SD = 9.9±7.9 vs. 11.9±8.7, p<0.0001), higher number of prior biologic DMARDs (1.3±1.1 vs. 1.0±1.0, p<0.0001) and lower DAS28 at baseline (5.1±1.7 vs. 5.7±1.5, p<0.0001). 16% of females and 42% of males were smokers (p<0.0001). 84% of smokers and 78% of non-smokers were anti-CCP positive (p=0.04).
Smokers had less improvement in disease activity than non-smokers at 6 months follow-up (mean±SD DeltaDAS28 -1.5±1.7 vs. -1.8±1.7, respectively, p=0.01). However, the difference was no longer significant after adjustment for baseline differences (age, sex, disease duration, number of prior biologic DMARDs, concomitant corticosteroids and DMARDs; p=0.40). When the analysis was stratified by anti-CCP status, smoking did not influence the response to therapy in the anti-CCP negative subset (p=0.39) but there was a trend in the anti-CCP positive subset (p=0.06, see figure 1). Similar trends were observed for EULAR good/moderate response rates. For the anti-CCP negative RA patients, 63% of non-smokers and 60% of smokers achieved EULAR response (p=0.51), while in the anti-CCP positive subgroup the respective response rates were 73% among non-smokers and 67% among smokers (p=0.07).
Conclusion: Smoking was negatively associated with the clinical response to rituximab therapy in RA patients who were anti-CCP positive.
M. L. Hetland,
Roche, Merck, and Abbvie,
Roche, Abbvie, Pfizer, BMS, Sanofi-Aventis, Merck, AB2 Bio,
P. van Riel,
J. J. Gomez-Reino,
Bristol-Myers Squibb, Pfizer Inc, Roche, Schering-Plough, and UCB SA,
Bristol-Myers Squibb, Roche, Schering-Plough, and Wyeth,
Roche and Schering-Plough,
T. K. Kvien,
R. F. van Vollenhoven,
AbbVie, BMS, GSK, Pfizer, Roche, UCB,
AbbVie, Biotest, BMS, Crescendo, GSK, Janssen, Lilly, Merck, Pfizer, Roche, UCB, Vertex,
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ACR Meeting Abstracts - https://acrabstracts.org/abstract/smoking-and-response-to-rituximab-in-anti-ccp-positive-and-negative-rheumatoid-arthritis-results-from-an-international-european-collaboration/