title: Rates of hospitalized bacterial infection associated with juvenile idiopathic arthritis and its treatment.
abstract: OBJECTIVE
  To compare the incidence of hospitalized bacterial infections among children with and children without juvenile idiopathic arthritis (JIA) and to examine the effects of selected medications.
  
  
  METHODS
  Using national Medicaid data from 2000 through 2005, we identified a cohort of children with JIA and a comparator cohort of children with attention deficit hyperactivity disorder (ADHD). Exposures to methotrexate (MTX), TNF inhibitors, and oral glucocorticoids (GCs) were determined using pharmacy claims. Patients hospitalized with bacterial infections were identified using coded discharge diagnoses. We calculated adjusted hazard ratios (HR(adj) ) to compare infection incidence rates while adjusting for relevant covariates.
  
  
  RESULTS
  We identified 8,479 JIA patients with 13,003 person-years of followup; 36% took MTX and 16% took TNF inhibitors. Compared with ADHD patients, JIA patients who were not currently taking MTX or TNF inhibitors had an increased rate of infection (HR(adj)  2.0 [95% confidence interval (95% CI) 1.5, 2.5]). Among JIA patients not receiving TNF inhibitor therapy, MTX users had a similar rate of infection as those not currently taking MTX (HR(adj)  1.2 [95% CI 0.9, 1.7]). TNF inhibitor use (irrespective of MTX) resulted in a similar rate of infection as use of MTX without a TNF inhibitor (HR(adj)  1.2 [95% CI 0.8, 1.8]). Use of high-dose GCs (≥10 mg/day of prednisone or equivalent) increased the rate of infection as compared with no GC use, after adjustment for MTX and TNF inhibitor use (HR(adj)  3.1 [95% CI 2.0, 4.7]).
  
  
  CONCLUSIONS
  Children with JIA had an increased rate of infection compared to children with ADHD. Among children with JIA, the rate of infection was not increased with MTX or TNF inhibitor use, but was significantly increased with high-dose GC use.
authors.affiliation: University of Alabama at Birmingham, Division of Pediatric Rheumatology, 1600 7th Avenue South, CPP 210, Birmingham, AL 35233-1711, USA. tbeukelman@peds.uab.edu
authors.forename: Timothy
authors.initials: T
authors.lastname: Beukelman
authors.forename: Fenglong
authors.initials: F
authors.lastname: Xie
authors.forename: Lang
authors.initials: L
authors.lastname: Chen
authors.forename: John W
authors.initials: JW
authors.lastname: Baddley
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Delzell
authors.forename: Carlos G
authors.initials: CG
authors.lastname: Grijalva
authors.forename: James D
authors.initials: JD
authors.lastname: Lewis
authors.forename: Rita
authors.initials: R
authors.lastname: Ouellet-Hellstrom
authors.forename: Nivedita M
authors.initials: NM
authors.lastname: Patkar
authors.forename: Kenneth G
authors.initials: KG
authors.lastname: Saag
authors.forename: Kevin L
authors.initials: KL
authors.lastname: Winthrop
authors.forename: Jeffrey R
authors.initials: JR
authors.lastname: Curtis
mesh_terms: D000293:Adolescent; D001171:Arthritis, Juvenile / Q000188:drug therapy* / Q000453:epidemiology*; D001424:Bacterial Infections / Q000453:epidemiology*; D002648:Child; D002675:Child, Preschool; D015331:Cohort Studies; D015897:Comorbidity; D004305:Dose-Response Relationship, Drug; D005260:Female; D005500:Follow-Up Studies; D005938:Glucocorticoids / Q000627:therapeutic use*; D006760:Hospitalization / Q000706:statistics & numerical data*; D006801:Humans; D015994:Incidence; D008297:Male; D008484:Medicaid; D008727:Methotrexate / Q000627:therapeutic use*; D011241:Prednisone / Q000627:therapeutic use; D012189:Retrospective Studies; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D014481:United States
chemical_list: D005938:Glucocorticoids; D014409:Tumor Necrosis Factor-alpha; D011241:Prednisone; D008727:Methotrexate