title: Presentation and outcome of histoplasmosis in pediatric inflammatory bowel disease patients treated with antitumor necrosis factor alpha therapy: a case series.
abstract: BACKGROUND
  Antitumor necrosis factor alpha (aTNF) therapies are commonly used in the treatment of pediatric inflammatory bowel disease (IBD). However, inhibition of the TNF-alpha pathway predisposes to serious infections, including histoplasmosis, which is the most common invasive fungal infection in individuals on aTNF therapy and carries a high mortality rate when associated with delayed diagnosis. Few data exist on the frequency, presentation, and appropriate treatment of pediatric patients with histoplasmosis on aTNF therapy.
  
  
  METHODS
  Following Institutional Review Board approval, cases were identified then reviewed with their primary gastroenterologist and infectious disease specialists.
  
  
  RESULTS
  Herein we describe histoplasmosis in five pediatric patients receiving aTNF therapy for IBD in an endemic area.
  
  
  CONCLUSIONS
  Histoplasmosis is an important complication of treatment with TNF-alpha neutralizing agents. Children with IBD treated with aTNF therapy who develop the infection may present with minimal pulmonary symptoms. While discontinuation of aTNF therapy is important initially, few data exist to determine when and how aTNF therapy can be reinstituted. Recognition of Histoplasma capsulatum is often delayed due to the overlap of symptoms with some of the extraintestinal manifestations of IBD and other more prevalent infectious complications.
authors.affiliation: Nationwide Children's Hospital, Columbus, Ohio 43205, USA. Jenniferdotson@nationwidechildrens.org
authors.forename: Jennifer L
authors.initials: JL
authors.lastname: Dotson
authors.forename: Wallace
authors.initials: W
authors.lastname: Crandall
authors.forename: Hayat
authors.initials: H
authors.lastname: Mousa
authors.forename: Jonathan R
authors.initials: JR
authors.lastname: Honegger
authors.forename: Lee
authors.initials: L
authors.lastname: Denson
authors.forename: Charles
authors.initials: C
authors.lastname: Samson
authors.forename: Dennis
authors.initials: D
authors.lastname: Cunningham
authors.forename: Jane
authors.initials: J
authors.lastname: Balint
authors.forename: Molly
authors.initials: M
authors.lastname: Dienhart
authors.forename: Preeti
authors.initials: P
authors.lastname: Jaggi
authors.forename: Ryan
authors.initials: R
authors.lastname: Carvalho
mesh_terms: D000068879:Adalimumab; D000293:Adolescent; D000328:Adult; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D061067:Antibodies, Monoclonal, Humanized; D000935:Antifungal Agents / Q000627:therapeutic use; D019353:Endemic Diseases; D005260:Female; D016469:Fungemia / Q000175:diagnosis* / Q000188:drug therapy / Q000382:microbiology; D006658:Histoplasma / Q000472:pathogenicity*; D006660:Histoplasmosis / Q000175:diagnosis* / Q000188:drug therapy / Q000382:microbiology; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000188:drug therapy* / Q000382:microbiology / Q000473:pathology; D000069285:Infliximab; D008172:Lung Diseases, Fungal / Q000175:diagnosis* / Q000188:drug therapy / Q000382:microbiology; D008297:Male; D014057:Tomography, X-Ray Computed; D016896:Treatment Outcome; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*; D055815:Young Adult
chemical_list: D000893:Anti-Inflammatory Agents; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D000935:Antifungal Agents; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000068879:Adalimumab