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Helicobacter pylori Infection and its Relationship with Histological Features of Gastric Mucosa in Patients with Early and Advanced Gastric Cancer

Matsukura Nori

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Abstract

Background: It has been confirmed that the development of gastric cancer spans over several decades sequentially starting with Helicobacter pylori () infection, and then, chronic active gastritis, atrophy and intestinal metaplasia. Finally, gastric cancer will eventually arise in a subset of these patients. Aims: To evaluateinfection and its relationship with the histological features of gastric mucosa in patients with normal endoscopy, chronic gastritis, early and advanced gastric cancer. Methods: The biopsy specimens were taken from the greater curvature of antrum, greater curvature of corpus and the angulus, respectively. HE staining, Giemsa staining and -specific antibody immunohistochemical staining were performed for histological diagnosis of infection, chronic gastritis with atrophy and intestinal metaplasia, as well as early or advanced gastric cancer. Results: The overall prevalence ofinfection in chronic gastritis, early and advanced gastric cancer patients was significantly higher than that in patients with normal endoscopy (52.4%, 52.4% and 81.2% vs. 44.9%, P0.05). There was no obvious difference ofinfection rate between chronic gastritis and early gastric cancer, but both were lower than that of advanced gastric cancer (P0.05). In endoscopically normal and chronic gastritis patients, the positivity rates of inflammation, atrophy and intestinal metaplasia in gastric mucosa were significantly higher in those withinfection than in those without (P0.05), and no differences were found in patients with early and advanced gastric cancer. Conclusions: Chronic inflammation, atrophy and intestinal metaplasia of the gastric mucosa induced byinfection possibly have direct and/or indirect effects on the development of gastric cancer.

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Background: It has been confirmed that the development of gastric cancer spans over several decades sequentially starting with Helicobacter pylori () infection, and then, chronic active gastritis, atrophy and intestinal metaplasia. Finally, gastric cancer will eventually arise in a subset of these patients. Aims: To evaluateinfection and its relationship with the histological features of gastric mucosa in patients with normal endoscopy, chronic gastritis, early and advanced gastric cancer. Methods: The biopsy specimens were taken from the greater curvature of antrum, greater curvature of corpus and the angulus, respectively. HE staining, Giemsa staining and -specific antibody immunohistochemical staining were performed for histological diagnosis of infection, chronic gastritis with atrophy and intestinal metaplasia, as well as early or advanced gastric cancer. Results: The overall prevalence ofinfection in chronic gastritis, early and advanced gastric cancer patients was significantly higher than that in patients with normal endoscopy (52.4%, 52.4% and 81.2% vs. 44.9%, P0.05). There was no obvious difference ofinfection rate between chronic gastritis and early gastric cancer, but both were lower than that of advanced gastric cancer (P0.05). In endoscopically normal and chronic gastritis patients, the positivity rates of inflammation, atrophy and intestinal metaplasia in gastric mucosa were significantly higher in those withinfection than in those without (P0.05), and no differences were found in patients with early and advanced gastric cancer. Conclusions: Chronic inflammation, atrophy and intestinal metaplasia of the gastric mucosa induced byinfection possibly have direct and/or indirect effects on the development of gastric cancer.

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Available abstract

Background: It has been confirmed that the development of gastric cancer spans over several decades sequentially starting with Helicobacter pylori () infection, and then, chronic active gastritis, atrophy and intestinal metaplasia. Finally, gastric cancer will eventually arise in a subset of these patients. Aims: To evaluateinfection and its relationship with the histological features of gastric mucosa in patients with normal endoscopy, chronic gastritis, early and advanced gastric cancer. Methods: The biopsy specimens were taken from the greater curvature of antrum, greater curvature of corpus and the angulus, respectively. HE staining, Giemsa staining and -specific antibody immunohistochemical staining were performed for histological diagnosis of infection, chronic gastritis with atrophy and intestinal metaplasia, as well as early or advanced gastric cancer. Results: The overall prevalence ofinfection in chronic gastritis, early and advanced gastric cancer patients was significantly higher than that in patients with normal endoscopy (52.4%, 52.4% and 81.2% vs. 44.9%, P0.05). There was no obvious difference ofinfection rate between chronic gastritis and early gastric cancer, but both were lower than that of advanced gastric cancer (P0.05). In endoscopically normal and chronic gastritis patients, the positivity rates of inflammation, atrophy and intestinal metaplasia in gastric mucosa were significantly higher in those withinfection than in those without (P0.05), and no differences were found in patients with early and advanced gastric cancer. Conclusions: Chronic inflammation, atrophy and intestinal metaplasia of the gastric mucosa induced byinfection possibly have direct and/or indirect effects on the development of gastric cancer.

Key concepts: Intestinal metaplasia, Medicine, Chronic gastritis, Cancer, Gastroenterology, Helicobacter pylori, Internal medicine, Gastritis

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