The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2006
PCNA expression in chronic gastritis due to Helicobacter pylori*.
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Akbulut Metin, Demirkan Neşe, Düzcan Ender
Аннотация
BACKGROUND/AIMS: It has been reported that cases of Helicobacter pylori (H. pylori) gastritis, those with epithelial hyperproliferation, have potential for malignant transformation. This study was planned to determine the effects of H. pylori on gastritis and the gastric epithelial cell proliferation.
METHODS: In this study, we re-evaluated biopsy samples obtained from 331 cases of chronic gastritis according to Sydney criteria, retrospectively. We examined the gastric epithelial cell proliferation with proliferating cell nuclear antigen in the proliferating zone, in the whole mucosa of intestinal metaplasia and in areas of regenerative atypia, separately.
RESULTS: The relationship between H. pylori colonization density and chronic active gastritis was statistically significant. We did not see any relationship between the presence and density of H. pylori in gastric mucosa via proliferating cell nuclear antigen indices. In the presence of lymphoid follicles, we noted a significant expression of proliferating cell nuclear antigen in the areas of whole gastric mucosa and regenerative atypia.
CONCLUSIONS: In the presence of lymphoid follicles, proliferating cell nuclear antigen expression was observed in the areas of whole gastric mucosa and regenerative atypia, but we did not see any relationship between the presence and density of H. pylori in gastric mucosa via proliferating cell nuclear antigen indices. This observation suggests the role of chronic inflammatory cells in gastric epithelial cell proliferation rather than the bacterium itself.
METHODS: In this study, we re-evaluated biopsy samples obtained from 331 cases of chronic gastritis according to Sydney criteria, retrospectively. We examined the gastric epithelial cell proliferation with proliferating cell nuclear antigen in the proliferating zone, in the whole mucosa of intestinal metaplasia and in areas of regenerative atypia, separately.
RESULTS: The relationship between H. pylori colonization density and chronic active gastritis was statistically significant. We did not see any relationship between the presence and density of H. pylori in gastric mucosa via proliferating cell nuclear antigen indices. In the presence of lymphoid follicles, we noted a significant expression of proliferating cell nuclear antigen in the areas of whole gastric mucosa and regenerative atypia.
CONCLUSIONS: In the presence of lymphoid follicles, proliferating cell nuclear antigen expression was observed in the areas of whole gastric mucosa and regenerative atypia, but we did not see any relationship between the presence and density of H. pylori in gastric mucosa via proliferating cell nuclear antigen indices. This observation suggests the role of chronic inflammatory cells in gastric epithelial cell proliferation rather than the bacterium itself.