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Abstract Number: 2524

Smoking and Response to Rituximab in Anti-CCP Positive and Negative Rheumatoid Arthritis – Results from an International European Collaboration

Katerina Chatzidionysiou1, Elisabeth Lie2, Evgeny Nasonov3, Galina Lukina3, Merete Lund Hetland4, Ellen Hauge5, Karel Pavelka6, Cem Gabay7, Dan Nordström8, Helena Canhão9, Matija Tomsic10, Piet van Riel11, Juan J. Gomez-Reino12, Ioan Ancuta13, Tore K. Kvien14, Ronald F. van Vollenhoven15 and Saedis Saevarsdottir16, 1Dept of Medicine, Unit for Clinical Research Therapy. Inflammatory Diseases (ClinTrid), Karolinska Institute, Stockholm, Sweden, 2Dept. of Rheumatology, Diakonhjemmet Hospital, Oslo, Norway, 3ARBITER, Institute of Rheumatology, Moscow, Russia, 4DANBIO, Center for Rheumatology and Spine Diseases, Glostrup University Hospital, Glostrup, Denmark, Glostrup, Denmark, 5Department of Rheumatology, Aarhus University Hospital, Aarhus, Denmark, 6Institute of Rheumatology and Department of Rheumatology, 1st Faculty of Medicine, Charles University in Prague, Prague, Czech Republic, 7SCQM registry, University Hospitals of Geneva, Geneva, Switzerland, 8ROB-FIN, Helsinki University Central Hospital, Helsinki, Finland, 9Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa and Rheumatology Department, Centro Hospitalar de Lisboa Norte, EPE, Hospital de Santa Maria, Lisboa, Portugal, 10Department of Rheumatology, University Medical Centre Ljubljana, Ljubljana, Slovenia, Ljubljana, Slovenia, 11Rheumatology, Radboud University Nijmegen Medical Centre, Nijmegen, Netherlands, 12Rheumatology, Hospital Clinico Universitario, Santiago, Spain, 13“Dr. I. Cantacuzino” Hospital, Bucharest, Romania, 14Rheumatology, Diakonhjemmet Hospital, Oslo, Norway, 15Unit for clinical therapy research (ClinTrid), Karolinska Institute, Stockholm, Sweden, 16Rheumatology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: rheumatoid arthritis (RA) and rituximab

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Session Information

Title: Rheumatoid Arthritis - Small Molecules, Biologics and Gene Therapy: Therapeutic Strategies, Biomarkers and Predictors of Outcomes in Rheumatoid Arthritis

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.  


Disclosure:

K. Chatzidionysiou,
None;

E. Lie,

AbbVie,

5,

UCB,

5,

Bristol-Myers Squibb,

5,

Hospira,

5,

Pfizer Inc,

5,

AbbVie,

8,

UCB,

8;

E. Nasonov,
None;

G. Lukina,
None;

M. L. Hetland,
None;

E. Hauge,
None;

K. Pavelka,
None;

C. Gabay,

Roche, Merck, and Abbvie,

2,

Roche, Abbvie, Pfizer, BMS, Sanofi-Aventis, Merck, AB2 Bio,

8;

D. Nordström,

Roche Pharmaceuticals,

9;

H. Canhão,
None;

M. Tomsic,
None;

P. van Riel,
None;

J. J. Gomez-Reino,

Bristol-Myers Squibb, Pfizer Inc, Roche, Schering-Plough, and UCB SA,

9,

Bristol-Myers Squibb, Roche, Schering-Plough, and Wyeth,

9,

Roche and Schering-Plough,

2;

I. Ancuta,
None;

T. K. Kvien,
None;

R. F. van Vollenhoven,

AbbVie, BMS, GSK, Pfizer, Roche, UCB,

2,

AbbVie, Biotest, BMS, Crescendo, GSK, Janssen, Lilly, Merck, Pfizer, Roche, UCB, Vertex,

5;

S. Saevarsdottir,
None.

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