title: Clinical response within 12 weeks as a predictor of future low disease activity in patients with early RA: results from the TEAR Trial.
abstract: OBJECTIVE
  Rapidly predicting future outcomes based on short-term clinical response would be helpful to optimize rheumatoid arthritis (RA) management in early disease. Our aim was to derive and validate a clinical prediction rule to predict low disease activity (LDA) at 1 year among patients participating in the Treatment of Early Aggressive Rheumatoid Arthritis (TEAR) trial escalating RA therapy by adding either etanercept or sulfasalazine + hydroxychloroquine [triple therapy (TT)] after 6 months of methotrexate (MTX) therapy.
  
  
  METHODS
  Eligible subjects included in the derivation cohort (used for model building, n = 186) were participants with moderate or higher disease activity [Disease Activity Score 28-erythrocyte sedimentation rate (DAS-ESR) > 3.2] despite 24 weeks of MTX monotherapy who added either etanercept or sulfasalazine + hydroxychloroquine. Clinical characteristics measured within the next 12 weeks were used to predict LDA 1 year later using multivariable logistic regression. Validation was performed in the cohort of TEAR patients randomized to initially receive either MTX + etanercept or TT.
  
  
  RESULTS
  The derivation cohort yielded 3 prediction models of varying complexity that included age, DAS28 at various timepoints, body mass index, and ESR (area under the receiver-operator characteristic curve up to 0.83). Accuracy of the prediction models ranged between 80% and 95% in both derivation and validation cohorts, depending on the complexity of the model and the cutpoints chosen for response and nonresponse. About 80% of patients could be predicted to be responders or nonresponders at Week 12.
  
  
  CONCLUSIONS
  Clinical data collected early after starting or escalating disease-modifying antirheumatic drug/biologic treatment could accurately predict LDA at 1 year in patients with early RA. For patients predicted to be nonresponders, treatment could be changed at 12 weeks to optimize outcomes.
authors.affiliation: From the University of Alabama at Birmingham, Birmingham, Alabama, USA. jcuirtis@uab.edu
authors.forename: Jeffrey R
authors.initials: JR
authors.lastname: Curtis
authors.forename: Theresa
authors.initials: T
authors.lastname: McVie
authors.forename: Ted R
authors.initials: TR
authors.lastname: Mikuls
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Reynolds
authors.forename: Iris
authors.initials: I
authors.lastname: Navarro-Millán
authors.forename: James
authors.initials: J
authors.lastname: O'Dell
authors.forename: Larry W
authors.initials: LW
authors.lastname: Moreland
authors.forename: S Louis
authors.initials: SL
authors.lastname: Bridges
authors.forename: Veena K
authors.initials: VK
authors.lastname: Ranganath
authors.forename: Stacey S
authors.initials: SS
authors.lastname: Cofield
mesh_terms: D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000175:diagnosis* / Q000188:drug therapy* / Q000503:physiopathology; D018450:Disease Progression; D004359:Drug Therapy, Combination; D000068800:Etanercept; D005260:Female; D006304:Health Status; D006801:Humans; D006886:Hydroxychloroquine / Q000627:therapeutic use; D007074:Immunoglobulin G / Q000627:therapeutic use; D008297:Male; D008727:Methotrexate / Q000627:therapeutic use; D008875:Middle Aged; D011379:Prognosis; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D012720:Severity of Illness Index; D012460:Sulfasalazine / Q000627:therapeutic use; D063189:Symptom Assessment / Q000379:methods; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D012460:Sulfasalazine; D006886:Hydroxychloroquine; D000068800:Etanercept; D008727:Methotrexate
keywords: ETANERCEPT; PREDICTION; RHEUMATOID ARTHRITIS; TRIPLE THERAPY; TUMOR NECROSIS FACTOR INHIBITOR