title: Can pre-neoplastic lesions be detected in gastric biopsies of children with Helicobacter pylori infection?
abstract: BACKGROUND
  Active gastritis, gastric mucosal atrophy and intestinal metaplasia are lesions associated with Helicobacter pylori infection. Atrophy and intestinal metaplasia are only seen in adults.
  
  
  OBJECTIVE
  We describe pediatric patients with atrophy and metaplasia, and compare the inflammatory response in these patients to controls.
  
  
  METHODS
  As part of a multicenter study of pediatric H. pylori infection, gastric biopsy specimens obtained during diagnostic upper endoscopy of 19 H. pylori-infected children and 45 uninfected controls were reviewed and graded by using the updated Sydney system. The inflammatory response was characterized using immunohistochemistry for T lymphocytes, B lymphocytes, and macrophages, and TUNEL assay for apoptosis.
  
  
  RESULTS
  Histology of H. pylori-infected and control biopsy specimens showed active gastritis in 32% and 2% respectively (P = 0.002). Mild intestinal metaplasia was found in 4 H. pylori-infected children, in two of whom it appeared to be accompanied by atrophy. Specimens from patients with H. pylori infection contained increased numbers of B lymphocytes in lymphoid nodules, and apoptosis in the superficial epithelium and inflammatory cells. T lymphocytes and macrophages appeared in similar numbers in specimens from controls and infected patients.
  
  
  CONCLUSIONS
  We describe intestinal metaplasia associated with H. pylori infection in children. Since atrophy usually precedes intestinal metaplasia in adults, we suggest that atrophy exists in children. High numbers of B lymphocytes and apoptosis in the surface epithelium are seen in patients with H. pylori infection and may be related to the development of atrophy and intestinal metaplasia.
authors.affiliation: Infectious Disease Pathology Activity, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta GA 30333, USA. jguarner@cdc.gov
authors.forename: Jeannette
authors.initials: J
authors.lastname: Guarner
authors.forename: Jeanine
authors.initials: J
authors.lastname: Bartlett
authors.forename: Toni
authors.initials: T
authors.lastname: Whistler
authors.forename: Daphne
authors.initials: D
authors.lastname: Pierce-Smith
authors.forename: Marilyn
authors.initials: M
authors.lastname: Owens
authors.forename: Rachel
authors.initials: R
authors.lastname: Kreh
authors.forename: Steven
authors.initials: S
authors.lastname: Czinn
authors.forename: Benjamin D
authors.initials: BD
authors.lastname: Gold
mesh_terms: D000293:Adolescent; D017209:Apoptosis; D001284:Atrophy; D001402:B-Lymphocytes / Q000276:immunology / Q000473:pathology; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D005260:Female; D005757:Gastritis, Atrophic / Q000276:immunology / Q000382:microbiology / Q000473:pathology; D016481:Helicobacter Infections / Q000276:immunology / Q000473:pathology*; D016480:Helicobacter pylori; D006801:Humans; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling / Q000379:methods; D007223:Infant; D007413:Intestinal Mucosa / Q000276:immunology / Q000382:microbiology / Q000473:pathology*; D008264:Macrophages / Q000276:immunology / Q000473:pathology; D008297:Male; D008679:Metaplasia; D011230:Precancerous Conditions / Q000473:pathology*; D013270:Stomach / Q000382:microbiology / Q000473:pathology*; D013274:Stomach Neoplasms / Q000473:pathology*; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology; D014510:Urease
chemical_list: D014510:Urease