Article Text

FRI0169 Smoking and Response to Rituximab in Anti-CCP Positive and Negative Rheumatoid Arthritis – Results from an International European Collaboration
  1. K. Chatzidionysiou1,
  2. E. Lie2,
  3. E. Nasonov3,
  4. G. Lukina3,
  5. M.L. Hetland4,
  6. E. Hauge5,
  7. K. Pavelka6,
  8. C. Gabay7,
  9. D. Nordström8,
  10. H. Canhão9,
  11. M. Tomsic10,
  12. P. van Riel11,
  13. J. Gomez-Reino12,
  14. I. Ancuta13,
  15. T. Kvien14,
  16. R. van Vollenhoven1,
  17. S. Saevarsdottir15
  1. 1ClinTRID, Karolinska Institute, Stockholm, Sweden
  2. 2Department of Rheumatology, Diakonhjemmet Hospita, Oslo, Norway
  3. 3ARBITER, Institute of Rheumatology, Moscow, Russian Federation
  4. 4DANBIO, Department of Rheumatology, Copenhagen University Hospital at Glostrup, Copenhagen
  5. 5Department of Rheumatology, Aarhus University Hospital, Aarhus, Denmark
  6. 6Charles University, Prague, Czech Republic
  7. 7SCQM registry, University Hospital of Geneva, Geneva, Switzerland
  8. 8ROB-FIN Helsinki University Central Hospital, Helsinki, Finland
  9. 9Rheumatology Research Unit, Instituto de Medicina Molecular, on behalf of the Rheumatic Diseases Portuguese Register, Lisbon, Portugal
  10. University Medical Center, Ljubljana, Slovenia
  11. 11Radboud University Nijmegen Medical Centre, Nijmegen, Netherlands
  12. 12Hosp Clinico Univ De Santiago, Santiago, Spain
  13. 13Cantacuzino Hospital, Bucharest, Romania
  14. 14Department of Rheumatology, Diakonhjemmet Hospital, Oslo, Norway
  15. 15Rheumatology Department, Karolinska University Hospital, Stockholm, Sweden


Background Smoking is a negative predictor of response to antirheumatic therapy.

Objectives To assess whether smoking influence the response to rituximab (RTX) in Rheumatoid Arthritis (RA).

Methods Pooled data from the Collaborating European Registries for RTX in RA (CERERRA) were used. Patients who received at least 1 cycle with RTX were included. Smoking status was defined as smokers (current smokers) and non-smokers (never and ex-smokers). 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 2274 patients were included - 1815 (80%) non-smokers and 459 (20%) smokers. 81% were female and 80% (out of 1199 patients with available anti-CCP) were anti-CCP positive. Smokers had shorter disease duration than non-smokers (median (IQR) 8 (4-13) years vs. 10 (5-16), p<0.0001), higher number of prior biologic DMARDs (median (IQR) 1 (0-2) vs. 1 (0-1), p<0.0001) and lower DAS28 at baseline (5.3±1.6 vs. 5.8±1.5, p<0.0001).

Smokers had less improvement in disease activity than non-smokers at 6 months (mean ± SD DeltaDAS28 -1.5±1.7 vs. -1.8±1.7, respectively, p=0.04). However, the difference was no longer significant after adjustment for baseline differences (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, figure 1). For the anti-CCP negative patients, 67% of non-smokers and 69% of smokers achieved EULAR response (p=0.6), while in the anti-CCP positive the respective response rates were 76% among non-smokers and 70% among smokers (p=0.09).

Conclusions Smoking was negatively associated with the response to rituximab therapy in RA patients who were anti-CCP positive.


  1. Khan A. et al. Smoking, rheumatoid factor status and responses to rituximab. Ann Rheum Dis 2012;71:1587-1588 doi:10.1136/annrheumdis-2012-201758

  2. Saevarsdottir S. et al. Patients with early rheumatoid arthritis who smoke are less likely to respond to treatment with methotrexate and tumor necrosis factor inhibitors: observations from the Epidemiological Investigation of Rheumatoid Arthritis and the Swedis Reumatology register cohorts. Arthritis Rheum 2011;63:26–36.

  3. Chatzidionysiou K. et al. Highest clinical effectiveness of rituximab in autoantibody-positive patients with rheumatoid arthritis and in those for whom no more than one previous TNF antagonist has failed. Pooled data from 10 European registries. Ann Rheum Dis 2011;70:1575–80.

Disclosure of Interest K. Chatzidionysiou: None declared, E. Lie: None declared, E. Nasonov: None declared, G. Lukina: None declared, M. Hetland: None declared, E. Hauge: None declared, K. Pavelka Consultant for: MSD, AbbVie, Pfizer, Roche, BMS, C. Gabay Grant/research support from: Roche, Merck, Abbvie, Consultant for: Roche, Abbvie, Pfizer, BMS, Sanofi-Aventis, Merck, AB2 Bio, D. Nordström Consultant for: AbbVie, BMS, MSD, Pfizer, Roche, UCB, H. Canhão: None declared, M. Tomsic: None declared, P. van Riel: None declared, J. Gomez-Reino: None declared, I. Ancuta: None declared, T. Kvien: None declared, R. van Vollenhoven Grant/research support from: AbbVie, BMS, GSK, Pfizer, Roche, UCB, Consultant for: AbbVie, Biotest, BMS, GSK, Janssen, Lilly, Merck, Pfizer, Roche, UCB, Vertex, S. Saevarsdottir: None declared

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