title: Attainment of inactive disease status following initiation of TNF-α inhibitor therapy for juvenile idiopathic arthritis: enthesitis-related arthritis predicts persistent active disease.
abstract: OBJECTIVE
  To analyze the attainment of inactive disease following initiation of tumor necrosis factor-α (TNF-α) inhibitors in a heterogeneous cohort of children with juvenile idiopathic arthritis (JIA).
  
  
  METHODS
  We performed retrospective chart review of all children with JIA at 1 academic center who had started TNF-α inhibitor therapy. We retrospectively determined inactive disease status according to the 2004 criteria of Wallace, et al. We evaluated inactive disease status at 1 year after initiation of TNF-α inhibitor and attainment of inactive disease at any point during the study period. Predictors of inactive disease were determined using univariate analyses and multivariable logistic regression models.
  
  
  RESULTS
  A total of 125 patients started TNF-α inhibitors, and 88 patients had data available for the 1-year followup visit. Many patients (49%) started TNF-α inhibitors within 6 months of the diagnosis of JIA. Diverse JIA phenotypes were represented: at baseline, 29% of all patients had active enthesitis and only 23% had active polyarthritis. At the 1-year followup, 36 of 88 (41%) patients had inactive disease. Overall, 67 of 125 (54%) patients ever attained inactive disease status during the study period. In multivariable models, enthesitis-related arthritis (ERA) and higher Childhood Health Assessment Questionnaire (CHAQ) scores at baseline were independently associated with failure to later attain inactive disease status.
  
  
  CONCLUSIONS
  Treatment with TNF-α inhibitors appears to be less effective for attaining inactive disease status in patients with ERA or higher baseline CHAQ scores. Further studies are needed regarding the clinical effectiveness of TNF-α inhibitor therapy and the optimal treatment of ERA.
authors.affiliation: University of Alabama School of Medicine, Birmingham, AL 35233, USA.
authors.forename: Katherine J
authors.initials: KJ
authors.lastname: Donnithorne
authors.forename: Randy Q
authors.initials: RQ
authors.lastname: Cron
authors.forename: Timothy
authors.initials: T
authors.lastname: Beukelman
mesh_terms: D000068879:Adalimumab; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized / Q000627:therapeutic use; D001171:Arthritis, Juvenile / Q000188:drug therapy* / Q000473:pathology* / Q000503:physiopathology*; D002675:Child, Preschool; D000068800:Etanercept; D005260:Female; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use; D007166:Immunosuppressive Agents / Q000627:therapeutic use*; D000069285:Infliximab; D008297:Male; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D012189:Retrospective Studies; D012216:Rheumatic Diseases / Q000473:pathology* / Q000503:physiopathology*; D012720:Severity of Illness Index; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D007074:Immunoglobulin G; D007166:Immunosuppressive Agents; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068879:Adalimumab; D000068800:Etanercept
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