Histopathology and expression of Ki-67 and cyclooxygenase-2 in childhood Helicobacter pylori gastritis

• Published in: Journal of gastroenterology Vol. 39; no. 3; pp. 231 - 237
• Main Authors: Kim, Kyung Mo, Oh, Young Lyun, Ko, Jae Sung, Choe, Yon Ho, Seo, Jeong Kee
• Format: Journal Article
• Language: English
• Published: Japan Springer Nature B.V 01-03-2004
• Subjects: Adolescent; Case-Control Studies; Child; Child, Preschool; Cyclooxygenase 2; Female; Gastric Mucosa - metabolism; Gastric Mucosa - pathology; Gastritis - enzymology; Gastritis - metabolism; Gastritis - microbiology; Gastritis - pathology; Helicobacter Infections - metabolism; Helicobacter Infections - pathology; Helicobacter pylori; Humans; Immunohistochemistry; Isoenzymes - metabolism; Ki-67 Antigen - metabolism; Male; Membrane Proteins; Prostaglandin-Endoperoxide Synthases - metabolism
• ISSN: 0944-1174; 1435-5922
• DOI: 10.1007/s00535-003-1282-9

Helicobacter pylori infection has been implicated in many pathobiologic changes that are linked with the pathogenesis of gastric cancer. The majority of studies have been performed in adults; however, H. pylori infection in children may be of greater significance because, in general, it reflects the early phase of infection. We therefore investigated several pathobiologic changes in the gastric mucosa of H. pylori-infected children, including histopathologic features, cell proliferation-associated Ki-67 antigen expression, and cyclooxygenase (COX)-2 expression.
Sixty-five children with nonulcer dyspepsia were included; 52 were infected with H. pylori, while the other 13 were free of H. pylori infection. A histopathologic review of biopsy specimens obtained from the gastric antrum was performed according to the updated Sydney system. Immunohistochemical expressions of Ki-67 and COX-2 were scored quantitatively or semiquantitatively.
The H. pylori-infected group was significantly associated with a higher grade of chronic inflammation, acute inflammation, and glandular atrophy. Ki-67 and COX-2 expressions were found to be significantly higher in the H. pylori-infected group. COX-2 expression was correlated with acute and chronic inflammation and Ki-67 expression. COX-2 expression was observed mainly in the monocytic cells and myofibroblasts in the lamina propria.
H. pylori-infected children, suggestive of the early phase of infection, exhibit increased gastric epithelial cell proliferation, increased COX-2 expression, and other pathobiologic features that may contribute to gastric carcinogenesis. These results have clinical significance for the early introduction of eradication of H. pylori infection in childhood.