title: Clinical activity after 12 weeks of treatment with nonbiologics in early rheumatoid arthritis may predict articular destruction 2 years later.
abstract: OBJECTIVE
  To investigate earlier prediction of future articular destruction in patients with early rheumatoid arthritis (RA).
  
  
  METHODS
  We randomly allocated patients with RA with disease duration < 2 years to different nonbiologic disease modifying antirheumatic drug (DMARD) therapies in a double-blind trial. Progression of articular destruction over the 96-week treatment period was assessed using the modified Sharp method.
  
  
  RESULTS
  Progression of articular destruction correlated more strongly with the American College of Rheumatology (ACR) core set measures after 12 weeks of treatment than with pretreatment values. Multiple regression analysis of data after 12 weeks yielded a correlation coefficient of 0.711. The sensitivity and specificity to predict articular destruction over the 75th percentile of the cohort were 78.6% and 84.6%, respectively. Patients who showed articular destruction over the 75th percentile of the cohort had low response to treatment at 12 weeks, and continued to have high clinical disease activity thereafter. Contrasting data were found in patients with slow progression of articular destruction.
  
  
  CONCLUSIONS
  In patients with early RA, ACR core set measures after 12 weeks of nonbiologic DMARD treatment may predict articular destruction 2 years later. Low response to treatment at 12 weeks and continuing high disease activity thereafter were found in patients with rapid radiological progression. These data can be used to determine the appropriateness of treatment at 12 weeks and aid the decision to introduce biologic DMARD.
authors.affiliation: Department of Rheumatic, Collagen and Allergic Diseases, St. Marianna University School of Medicine, Kawasaki, Japan.
authors.forename: Yoichi
authors.initials: Y
authors.lastname: Ichikawa
authors.forename: Terunobu
authors.initials: T
authors.lastname: Saito
authors.forename: Hisasi
authors.initials: H
authors.lastname: Yamanaka
authors.forename: Masashi
authors.initials: M
authors.lastname: Akizuki
authors.forename: Hirobumi
authors.initials: H
authors.lastname: Kondo
authors.forename: Shigeto
authors.initials: S
authors.lastname: Kobayashi
authors.forename: Hisaji
authors.initials: H
authors.lastname: Oshima
authors.forename: Shinichi
authors.initials: S
authors.lastname: Kawai
authors.forename: Nobuaki
authors.initials: N
authors.lastname: Hama
authors.forename: Hidehiro
authors.initials: H
authors.lastname: Yamada
authors.forename: Tsuneyo
authors.initials: T
authors.lastname: Mimori
authors.forename: Koichi
authors.initials: K
authors.lastname: Amano
authors.forename: Yasushi
authors.initials: Y
authors.lastname: Tanaka
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Matsuoka
authors.forename: Sumiki
authors.initials: S
authors.lastname: Yamamoto
authors.forename: Tsukasa
authors.initials: T
authors.lastname: Matsubara
authors.forename: Norikazu
authors.initials: N
authors.lastname: Murata
authors.forename: Tomiaki
authors.initials: T
authors.lastname: Asai
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Suzuki
mesh_terms: D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000188:drug therapy* / Q000473:pathology; D018450:Disease Progression; D004311:Double-Blind Method; D006801:Humans; D007596:Joints / Q000187:drug effects / Q000473:pathology*; D011237:Predictive Value of Tests; D011379:Prognosis; D012044:Regression Analysis; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D016896:Treatment Outcome
chemical_list: D018501:Antirheumatic Agents