SAT0147 Effect of smoking on response to therapy with TNF-A inhibitors for rheumatoid arthritis: Results from the corrona registry
Authors: O. Pala, S. Messing, A. Hopkins, G. Reed, M. Perez-Rivera, M. Acosta, J.M. Kremer, C. Lozada, D.A. Pappas
Journal: Annals of the Rheumatic Diseases (2013)

<h3>Background</h3> TNF-a inhibitors (TNFi) have revolutionized the therapy of Rheumatoid Arthritis (RA). However, up to 30% of patients fail to respond to treatment (tx) with TNFi or respond inadequately. Factors affecting response have been investigated, include smoking and suggest an unfavorable effect of smoking to TNFi tx. Data so far have been derived from small cohorts with some differences in the U.S and European patients. <h3>Objectives</h3> To evaluate the effect of smoking to response to tx with TNFi using the large cohort of patients participating in the Consortium of Rheumatology Researchers of North America (CORRONA). <h3>Methods</h3> The CORRONA registry is a network of over 100 private and academic rheumatology practices across the U.S with 30,537 RA patients. Mean duration of follow up (fu) per patient is 3.4 years (SD: 2.6). Enrolled patients have been followed for up to 10.2 years. Cumulative length of fu for all RA patients is 61,918 years. We identified biologic naïve patients and followed them for 6 months after initiation of a TNFi. We investigated the association of smoking status (current vs non current) with response to TNFi tx. Outcomes of interest included DAS28, CDAI, mHAQ and EULAR response criteria after six months on TNFi. Regression models to isolate the effect of smoking on outcomes included baseline values of the outcome of interest, age, gender, race, concurrent DMARD tx. <h3>Results</h3> 2811 naïve TNFi initiators with at least 6 months of fu were identified from registry inception until 12/2010. 521 of them were smokers at the time of TNFi initiation (baseline) and 2290 were not. Current smokers were slightly younger (mean age, SD: 53.2, 11.9) at baseline compared to non smokers (57.3, SD: 13.7) (p:&lt;0.0001) and were more likely to be on TNFi monotherapy (23.0% vs 18.7%) (p:0.03). All other baseline demographic and disease characteristics were balanced between smokers and non-smokers. Disease activity measures at baseline were similar for DAS28 (approximately 3.7, SD: 1.6) for both groups but higher for CDAI and mHAQ in smokers (17.1, SD: 13.8 vs 15.5, SD: 12.9 and 0.5, SD:0.5 vs 0.4, SD:0.4) respectively. Regression modeling results (Table) showed a significantly higher CDAI and DAS28 at 6 months among smokers. There was no significant difference in the odds of smokers vs non smokers in achieving at least moderate EULAR response at 6 months and no difference in the change of mHAQ. <h3>Conclusions</h3> Data from the CORRONA registry including thousands of US patients add to the existing evidence regarding the unfavorable influence of smoking to response with TNFi tx, even when starting with less severe disease. <h3>Disclosure of Interest</h3> O. Pala: None Declared, S. Messing: None Declared, A. Hopkins Employee of: University of Miami Miller School of Medicine, G. Reed Grant/Research support from: CORRONA, Consultant for: CORRONA, Employee of: University of Massachusetts Medical School, Paid Instructor for: Harvard Medical School, M. Perez-Rivera Employee of: University of Miami Miller School of Medicine, M. Acosta Employee of: University of Miami Miller School of Medicine, J. Kremer Shareholder of: CORRONA, Grant/Research support from: Abbott, Amgen, AstraZeneca, BMS, Genentech, Lilly, Pfizer, Consultant for: Amgen, Genentech, Lilly, Pfizer, Employee of: CORRONA, Speakers Bureau: Abbott, Amgen, BMS, Pfizer, C. Lozada: None Declared, D. Pappas: None Declared