title: Should we redefine treatment targets in rheumatoid arthritis? Low disease activity is sufficiently strict for patients who are anticitrullinated protein antibody-negative.
abstract: OBJECTIVE
  Clinical remission currently is the treatment target for all patients with rheumatoid arthritis (RA). At the same level of inflammation, the prognosis regarding joint damage is believed to be different for anticitrullinated protein antibody (ACPA)-negative and ACPA-positive patients. Our objective was to show the difference in prognosis at similar disease activity levels, and to illustrate how this could be translated to differentiation of treatment targets.
  
  
  METHODS
  Data were used from the Nijmegen Early RA Cohort. The relation between the time-averaged disease activity level (by Disease Activity Score; DAS) and joint damage progression over 3 years was analyzed, separately for ACPA-negative and ACPA-positive patients. Joint damage was assessed as change in Ratingen score, and dichotomized as occurrence of erosions in joints that were unaffected at baseline. Linear and logistic multivariable regression models were used.
  
  
  RESULTS
  The regression coefficient of DAS on change in Ratingen score was 3.9 (p < 0.001) for ACPA-negative and 4.7 (p < 0.001) for ACPA-positive patients, showing less joint damage progression at the same disease activity level in ACPA-negative patients. This difference became greater with increasing disease activity. The probability for erosions in joints unaffected at baseline was 0.35 in ACPA-negative patients when time-averaged DAS was < 2.4 versus 0.80 in ACPA-positive patients.
  
  
  CONCLUSIONS
  At the same level of inflammation, ACPA-negative patients have less joint damage and lower probability for damage in newly affected joints than ACPA-positive patients. Low disease activity might be a sufficiently strict treatment target for ACPA-negative patients to prevent progression of joint damage.
authors.affiliation: Department of Rheumatology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
authors.forename: Yvonne M R
authors.initials: YM
authors.lastname: de Punder
authors.forename: Jos
authors.initials: J
authors.lastname: Hendrikx
authors.forename: Alfons A
authors.initials: AA
authors.lastname: den Broeder
authors.forename: Elia
authors.initials: E
authors.lastname: Valls Pascual
authors.forename: Piet L
authors.initials: PL
authors.lastname: van Riel
authors.forename: Jaap
authors.initials: J
authors.lastname: Fransen
mesh_terms: D000328:Adult; D000368:Aged; D000888:Antibodies, Anti-Idiotypic / Q000097:blood*; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000175:diagnosis / Q000188:drug therapy* / Q000276:immunology*; D001175:Arthrography; D001799:Blood Sedimentation; D015331:Cohort Studies; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D016014:Linear Models; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D017063:Outcome Assessment, Health Care / Q000592:standards*; D010456:Peptides, Cyclic / Q000276:immunology*; D011379:Prognosis; D012189:Retrospective Studies; D012217:Rheumatoid Factor / Q000097:blood; D012720:Severity of Illness Index; D016896:Treatment Outcome
chemical_list: D000888:Antibodies, Anti-Idiotypic; D018501:Antirheumatic Agents; D010456:Peptides, Cyclic; C487763:cyclic citrullinated peptide; D012217:Rheumatoid Factor
keywords: ANTICITRULLINATED PROTEIN ANTIBODY; INFLAMMATION; JOINT EROSIONS; RHEUMATOID ARTHRITIS