title: The effect of smoking on response and drug survival in rheumatoid arthritis patients treated with their first anti-TNF drug.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  Current smoking was predictive of poor response to anti-TNF treatment for up to 12 months and heavy smokers had the poorest drug survival.
authors: Research and Development Centre, Spenshult Rheumatology Hospital, Oskarström, Sweden. maria.soderlin@spenshult.se
authors: M K
authors: MK
authors: Söderlin
authors: I F
authors: IF
authors: Petersson
authors: P
authors: P
authors: Geborek
mesh_terms: D000068879:Adalimumab; D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D001799:Blood Sedimentation; D002097:C-Reactive Protein / Q000378:metabolism; D015331:Cohort Studies; D000068800:Etanercept; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use; D000069285:Infliximab; D008297:Male; D008875:Middle Aged; D010147:Pain Measurement; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D012042:Registries; D012044:Regression Analysis; D012720:Severity of Illness Index; D012907:Smoking / Q000009:adverse effects*; D011795:Surveys and Questionnaires; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept