Özet:

Helicobacter pylori is considered a class I carcinogen by the World Health Organization. We aimed to determine whether H. pylori has an effect on telomerase activity in patients with H. pylori related non-specific gastritis, atrophy, and intestinal metaplasia. Materials and methods: One hundred and seventy-two adult patients who underwent upper gastroduodenoscopy were enrolled in the study. Three biopsy specimens were taken from the antrum: 1 from the incisura angularis and 2 from the mid-antrum. Biopsy specimens taken from the incisura angularis were evaluated using the urease test for detection of H. pylori. The mid-antrum specimens were sent for histopathology and tissue telomerase activity testing. The histopathologic evaluation was performed based on the updated Sydney system. Quantitative detection of hTERT mRNA was performed with the available method for telomerase activity. Results: Of the 172 patients, 119 were eligible for the study. H. pylori was positive in 68 (57.14%) and negative in 51 (42.85%) of the cases (P > 0.05). Of the 119 patients, 6 had intestinal metaplasia, 27 had glandular atrophy, 62 had neutrophilic activation, and 102 had chronic inflammation. The telomerase activity of the H. pylori positive and negative groups did not show a statistically significant difference in patients with intestinal metaplasia, glandular atrophy, neutrophilic activation, and chronic inflammation (P > 0.05, for each). hTERT activity was higher in H. pylori positive patients who had glandular atrophy and intestinal metaplasia than the negative group. However, the differences were insignificant. Conclusion: We could not find any significant relationship between telomerase activity and H. pylori related non-specific gastritis, atrophy, and intestinal metaplasia. hTERT activity was higher in patients who had glandular atrophy and intestinal metaplasia (early stages of gastric carcinogenesis) in the H. pylori positive group. However, these differences were not significant. H. pylori, which is considered an oncogenic agent, may influence telomerase activity of further stages of carcinogenesis, particularly those after intestinal metaplasia.

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