Helicobacter pylori infection is associated with an increased cell proliferation activity, however the exact mechanisms have not been elucidated. Our aim was to study the effect of Helicobacter pylori infection on normal gastric epithelia, gastritis, intestinal metaplasia and carcinoma by the expression of proliferating cell nuclear antigen and nucleolus organizer regions. Antral biopsies were taken from 121 patients (61 women, 60 men; mean age 58.5 y.). Sections were scored for normal epithelia (n = 15), gastritis without intestinal metaplasia (n = 74), gastritis with intestinal metaplasia (n = 24) and gastric carcinoma (n = 8). 52 patients had H. pylori positive gastritis, and success of eradication therapy was controlled in 34 cases. To characterize cell proliferation immunohistochemistry (PCNA) and histochemistry methods (AgNOR) were used. Results of PCNA and AgNOR significantly correlated except of that in the intestinal metaplasia group. PCNA LI and AgNOR counts were not significant higher in H. pylori positive compared to the H. pylori negative gastritis. Presence of H. pylori caused higher proliferation rate in intestinal metaplasia group measured by PCNA. In the group of intestinal metaplasia the proliferation activity decreased to the activity of the normal epithelia after the successful eradication, but remained high if eradication therapy was failed. Our results suggest, that H. pylori infection plays only as a co-factor in gastric carcinogenesis. Results were controversial in the intestinal metaplasia group, that can be explained by the heterogeneity of the bacteria.
|Translated title of the contribution||Effect of Helicobacter pylori infection and eradication on proliferative kinetics of the gastric mucosa|
|Number of pages||6|
|Publication status||Published - Dec 10 2000|
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