title: Impact of anti-TNF treatment on growth in severe juvenile idiopathic arthritis.
abstract: OBJECTIVE
  To evaluate the impact of anti-tumour necrosis factor (TNF) treatment on growth and to identify the predictors for the change in growth in severe juvenile idiopathic arthritis (JIA).
  
  
  METHODS
  Data from 71 JIA patients (43 on etanercept, 28 on infliximab) were reviewed two years before and two years on the anti-TNF treatment. The patients had polyarticular disease course (48 polyarthritis, 19 extended oligoarthritis, two systemic arthritis, and two enthesitis related arthritis). At the initiation of the anti-TNF treatment, their mean age was 9.6 years and the mean duration of JIA, 5.7 years.
  
  
  RESULTS
  In the patients with delayed growth before anti-TNF treatment (n = 53), the growth velocity, measured as the change in height standard deviation score, accelerated +0.45 (95% confidence interval, 0.33 to 0.56) (p<0.001) during the anti-TNF treatment. In the patients with normal or accelerated growth before anti-TNF treatment (n = 18), the change in growth velocity was +0.05 (0.07 to 0.16) (p = 0.39). At two years on anti-TNF treatment, the growth velocity between these two groups was similar. No difference was found between the patients treated with etanercept or infliximab. A decelerating growth rate before the anti-TNF treatment was the strongest predictor for the observed increase in the growth velocity. The change in the inflammatory activity remained a significant predictor of the growth velocity even after the decrease in glucocorticoid dose was taken into account.
  
  
  CONCLUSIONS
  In the treatment of polyarticular JIA, the anti-TNF treatment not only suppresses inflammation but also restores growth velocity.
authors.affiliation: Hospital for Children and Adolescents, Helsinki University Central Hospital, Research Unit, Lastenlinnantie 11 C 29, PL 280, 00029 HUS, Finland. pirjo.tynjala@hus.fi
authors.forename: P
authors.initials: P
authors.lastname: Tynjälä
authors.forename: P
authors.initials: P
authors.lastname: Lahdenne
authors.forename: P
authors.initials: P
authors.lastname: Vähäsalo
authors.forename: H
authors.initials: H
authors.lastname: Kautiainen
authors.forename: V
authors.initials: V
authors.lastname: Honkanen
mesh_terms: D000293:Adolescent; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D018501:Antirheumatic Agents / Q000627:therapeutic use*; D001171:Arthritis, Juvenile / Q000188:drug therapy* / Q000276:immunology / Q000503:physiopathology*; D001799:Blood Sedimentation; D001827:Body Height / Q000187:drug effects; D015992:Body Mass Index; D001835:Body Weight / Q000187:drug effects; D002097:C-Reactive Protein / Q000032:analysis; D016009:Chi-Square Distribution; D002648:Child; D000068800:Etanercept; D005260:Female; D006128:Growth / Q000187:drug effects*; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use; D000069285:Infliximab; D008297:Male; D008727:Methotrexate / Q000627:therapeutic use; D011446:Prospective Studies; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D012189:Retrospective Studies; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D000911:Antibodies, Monoclonal; D018501:Antirheumatic Agents; D007074:Immunoglobulin G; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D002097:C-Reactive Protein; D000069285:Infliximab; D000068800:Etanercept; D008727:Methotrexate