title: Tumour necrosis factor α blockers are more effective than methotrexate in the inhibition of radiographic joint damage progression among patients with psoriatic arthritis.
abstract: OBJECTIVE
  To determine whether tumour necrosis factor α (TNFα) blockers are more effective than methotrexate in inhibiting the progression of radiographic joint damage in patients with psoriatic arthritis (PsA).
  
  
  METHODS
  A cohort analysis of patients followed prospectively in a large PsA clinic was conducted. Patients who received a TNFα blocker were compared to those treated with methotrexate. Patients who had records of at least 12 months of treatment with either medication for active peripheral PsA and had radiographic bone erosions were analysed. Radiographs of the hands and feet were performed at baseline, 1-2 years (time 1) and 3-4 years (time 2). Radiographic joint damage was scored according to the modified Steinbrocker score. The outcome of interest was the occurrence of radiographic progression. Multivariate logistic regression analysis using generalised estimating equations for repeated measures was used to compare progression in radiographic joint damage between the two treatment groups.
  
  
  RESULTS
  65 patients treated with TNFα blockers and 70 patients treated with methotrexate were analysed. The proportion of patients who demonstrated progression of radiographic damage score at time 1 and time 2 was higher in the methotrexate group compared to the TNFα blockers group (at time 1: 80% vs 58.9% p=0.005; at time 2: 88% vs 61% p=0.005). In the multivariate regression analysis methotrexate treatment was associated with an increase in radiographic damage compared to TNFα blockers (p=0.001).
  
  
  CONCLUSIONS
  In a clinic setting, patients with erosive PsA receiving TNFα blockers had a better radiographic outcome compared to those treated with methotrexate.
authors.affiliation: University of Toronto Psoriatic Arthritis Clinic, Centre for Prognosis Studies in the Rheumatic Diseases, Toronto Western Hospital, , Toronto, Ontario, Canada.
authors.forename: Lihi
authors.initials: L
authors.lastname: Eder
authors.forename: Arane
authors.initials: A
authors.lastname: Thavaneswaran
authors.forename: Vinod
authors.initials: V
authors.lastname: Chandran
authors.forename: Dafna D
authors.initials: DD
authors.lastname: Gladman
mesh_terms: D000068879:Adalimumab; D000328:Adult; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D015535:Arthritis, Psoriatic / Q000000981:diagnostic imaging / Q000188:drug therapy*; D015331:Cohort Studies; D018450:Disease Progression; D000068800:Etanercept; D005260:Female; D033023:Foot Joints / Q000000981:diagnostic imaging*; D050823:Hand Joints / Q000000981:diagnostic imaging*; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use; D000069285:Infliximab; D016015:Logistic Models; D008297:Male; D008727:Methotrexate / Q000627:therapeutic use*; D008875:Middle Aged; D015999:Multivariate Analysis; D011446:Prospective Studies; D011859:Radiography; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; 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; C529000:golimumab; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept; D008727:Methotrexate
keywords: Anti-TNF; Psoriatic Arthritis; TNF-alpha