M K Söderlin1, I F Petersson, P Geborek. 1. Research and Development Centre, Spenshult Rheumatology Hospital, Oskarström, Sweden. maria.soderlin@spenshult.se
Abstract
OBJECTIVES: Smoking has been associated with higher disease activity and poor response to anti-tumour necrosis factor (anti-TNF) therapy in patients with rheumatoid arthritis (RA). We wanted to study the effect of smoking on response to therapy, disease activity measures, and drug survival in RA patients starting their first anti-TNF drug. METHODS: In 2005, RA patients in a voluntary rheumatology biologics register in Southern Sweden answered a questionnaire that included smoking habits. The primary endpoint comprised the European League Against Rheumatism (EULAR) response criteria at 3, 6, and 12 months. Secondary endpoints were the Simplified Disease Activity Index (SDAI), Clinical Disease Activity Index (CDAI) response criteria, and drug survival. RESULTS: Between 1999 and 2005, 23% of RA patients (216/934) in Southern Sweden were current smokers at the start of anti-TNF therapy. Smoking did not influence disease activity at baseline. Heavy smokers had the poorest drug survival. Current smoking was a negative predictive factor for EULAR response at the 3-month follow-up [odds ratio (OR) 0.53, 95% confidence interval (CI) 0.32-0.87, p = 0.012], and for SDAI response at 3 months (OR 0.45, 95% CI 0.27-0.77, p = 0.003) and 6 months (OR 0.47, 95% CI 0.25-0.88, p = 0.02). A pack-year history of 11-20 was a negative predictive factor for SDAI response at 12 months (OR 0.30, 95% CI 0.13-0.70, p = 0.005). Smokers had higher visual analogue scale (VAS) global scores, C-reactive protein (CRP) levels, and erythrocyte sedimentation rate (ESR) at 3 months. CONCLUSION: Current smoking was predictive of poor response to anti-TNF treatment for up to 12 months and heavy smokers had the poorest drug survival.
OBJECTIVES: Smoking has been associated with higher disease activity and poor response to anti-tumour necrosis factor (anti-TNF) therapy in patients with rheumatoid arthritis (RA). We wanted to study the effect of smoking on response to therapy, disease activity measures, and drug survival in RApatients starting their first anti-TNF drug. METHODS: In 2005, RApatients in a voluntary rheumatology biologics register in Southern Sweden answered a questionnaire that included smoking habits. The primary endpoint comprised the European League Against Rheumatism (EULAR) response criteria at 3, 6, and 12 months. Secondary endpoints were the Simplified Disease Activity Index (SDAI), Clinical Disease Activity Index (CDAI) response criteria, and drug survival. RESULTS: Between 1999 and 2005, 23% of RApatients (216/934) in Southern Sweden were current smokers at the start of anti-TNF therapy. Smoking did not influence disease activity at baseline. Heavy smokers had the poorest drug survival. Current smoking was a negative predictive factor for EULAR response at the 3-month follow-up [odds ratio (OR) 0.53, 95% confidence interval (CI) 0.32-0.87, p = 0.012], and for SDAI response at 3 months (OR 0.45, 95% CI 0.27-0.77, p = 0.003) and 6 months (OR 0.47, 95% CI 0.25-0.88, p = 0.02). A pack-year history of 11-20 was a negative predictive factor for SDAI response at 12 months (OR 0.30, 95% CI 0.13-0.70, p = 0.005). Smokers had higher visual analogue scale (VAS) global scores, C-reactive protein (CRP) levels, and erythrocyte sedimentation rate (ESR) at 3 months. CONCLUSION: Current smoking was predictive of poor response to anti-TNF treatment for up to 12 months and heavy smokers had the poorest drug survival.
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