title: Histopathology of gastritis in Helicobacter pylori-infected children from populations at high and low gastric cancer risk.
abstract: Infection with Helicobacter pylori has been recognized as a cause of gastric carcinoma. Although the neoplasia is always detected in adults, the infection starts in childhood. It has been reported that early age at first infection is a determinant of gastric cancer risk. In this study, we examined the histopathology of the gastric mucosa in infected children from a population at high risk for gastric cancer (Pasto, Colombia) and compared it with that of a lower-risk population (New Orleans, LA). Gastric biopsies obtained from antrum and corpus were stained with hematoxylin and eosin and Steiner's silver method. Immunohistochemical stains were used to identify B lymphocytes (CD20), T lymphocytes (CD3 and CD8), macrophages (CD68), and polymorphonuclear neutrophil myeloperoxidase. Morphometric techniques were used to evaluate the immunohistochemical stains. In both populations, the inflammatory lesions were seen predominantly in the antrum. Compared with children from the lower-risk populations, children from the higher-risk population exhibited more severe polymorphonuclear neutrophil infiltration, stromal and intraepithelial lymphocyte infiltration, mucus depletion, and H. pylori colonization density. Regenerative activity was significantly more marked in the lower-risk population. Morphometric analysis of immunohistochemical stains showed increased representation of T lymphocytes and macrophages in the higher-risk population. Most T lymphocytes stained positive for CD8, a marker of suppressor/cytotoxic cells. B lymphocytes were relatively more abundant in the lower-risk population. The possibility that the aforementioned characteristics of H. pylori infection in children are related to cancer risk in adults is discussed.
authors.affiliation: Hospital Infantil, Pasto, Colombia.
authors.forename: Alvaro
authors.initials: A
authors.lastname: Bedoya
authors.forename: Jone
authors.initials: J
authors.lastname: Garay
authors.forename: Fernando
authors.initials: F
authors.lastname: Sanzón
authors.forename: Luis E
authors.initials: LE
authors.lastname: Bravo
authors.forename: Juan C
authors.initials: JC
authors.lastname: Bravo
authors.forename: Hernan
authors.initials: H
authors.lastname: Correa
authors.forename: Randall
authors.initials: R
authors.lastname: Craver
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Fontham
authors.forename: Joanna X
authors.initials: JX
authors.lastname: Du
authors.forename: Pelayo
authors.initials: P
authors.lastname: Correa
mesh_terms: D001402:B-Lymphocytes / Q000473:pathology; D001706:Biopsy; D017252:CD3 Complex / Q000032:analysis; D016827:CD8 Antigens / Q000032:analysis; D002648:Child; D002675:Child, Preschool; D003105:Colombia / Q000453:epidemiology; D004848:Epithelium / Q000473:pathology; D005260:Female; D005753:Gastric Mucosa / Q000473:pathology; D005756:Gastritis / Q000382:microbiology* / Q000473:pathology*; D016481:Helicobacter Infections / Q000473:pathology*; D016480:Helicobacter pylori; D006801:Humans; D007150:Immunohistochemistry; D007223:Infant; D008145:Louisiana; D008264:Macrophages / Q000473:pathology; D008297:Male; D009504:Neutrophils / Q000201:enzymology / Q000473:pathology; D009195:Peroxidase / Q000032:analysis; D012307:Risk Factors; D013274:Stomach Neoplasms / Q000453:epidemiology / Q000382:microbiology*; D013601:T-Lymphocytes / Q000276:immunology / Q000473:pathology
chemical_list: D017252:CD3 Complex; D016827:CD8 Antigens; D009195:Peroxidase