title: Differential drug retention between anti-TNF agents and alternative biological agents after inadequate response to an anti-TNF agent in rheumatoid arthritis patients.
abstract: BACKGROUND
  After inadequate response to an antitumour necrosis factor (aTNF) agent for treatment of rheumatoid arthritis (RA), rheumatologists can choose an alternative aTNF or a biological agent with another mode of action (non-aTNF biological (non-aTNF-Bio)).
  
  
  OBJECTIVE
  To compare drug retention rates of non-aTNF-Bio with alternative aTNF.
  
  
  METHODS
  All patients within the Swiss RA cohort (SCQM-RA) treated with an alternative biotherapy after a prior inadequate response to aTNF were analysed. The drug retention of alternative aTNF was compared with non-aTNF-Bio using Cox proportional hazards models, adjusted for potential confounders.
  
  
  RESULTS
  1485 treatment courses after aTNF failure were available for analysis, 853 with alternative aTNF and 632 with non-aTNF-Bio. The median drug retention was 32 months (IQR 14-54) on non-aTNF-Bio versus 21 months (IQR 8-53) on alternative aTNF, or a 50% reduction drug discontinuation risk in favour of non-aTNF-Bio (adjusted hazard ratio (HR) for non-aTNF-Bio: 0.50 (95% CI 0.41 to 0.62)). This effect appears to be modified by the type of prior aTNF failure, with a larger difference in favour of non-aTNF-Bio in patients having experienced a primary failure with a previous aTNF (HR: 0.33 (95% CI 0.24 to 0.47), p<0.001).
  
  
  CONCLUSIONS
  After inadequate response to aTNF, and particularly after primary failure, patients on a non-aTNF-Bio agent have significantly higher drug retention rates.
authors.affiliation: Rheumatology, University Hospitals of Geneva, Geneva, Switzerland. Sophie.Martin-Du-Pan@hcuge.ch
authors.forename: Sophie Martin
authors.initials: SM
authors.lastname: Du Pan
authors.forename: Almut
authors.initials: A
authors.lastname: Scherer
authors.forename: Cem
authors.initials: C
authors.lastname: Gabay
authors.forename: Axel
authors.initials: A
authors.lastname: Finckh
mesh_terms: D000069594:Abatacept; D000068879:Adalimumab; D000328:Adult; D000368:Aged; D061067:Antibodies, Monoclonal, Humanized / Q000008:administration & dosage / Q000493:pharmacokinetics*; D018501:Antirheumatic Agents / Q000008:administration & dosage / Q000493:pharmacokinetics*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy*; D005260:Female; D005938:Glucocorticoids / Q000008:administration & dosage / Q000493:pharmacokinetics; D006801:Humans; D018796:Immunoconjugates / Q000008:administration & dosage / Q000493:pharmacokinetics*; D007555:Isoxazoles / Q000008:administration & dosage / Q000493:pharmacokinetics; D000077339:Leflunomide; D008297:Male; D008727:Methotrexate / Q000008:administration & dosage / Q000493:pharmacokinetics*; D008875:Middle Aged; D011241:Prednisone / Q000008:administration & dosage / Q000493:pharmacokinetics; D016016:Proportional Hazards Models; D012042:Registries; D012074:Remission Induction; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D061067:Antibodies, Monoclonal, Humanized; D018501:Antirheumatic Agents; D005938:Glucocorticoids; D018796:Immunoconjugates; D007555:Isoxazoles; D014409:Tumor Necrosis Factor-alpha; D000069594:Abatacept; D000068879:Adalimumab; D000077339:Leflunomide; D011241:Prednisone; D008727:Methotrexate