Effect of Helicobacter pylori Infection on Pathologic Changes of Gastric Mucosa
Dong‐Tsamn Lin
Abstract
Dong‐Tsamn Lin
Abstract
Background: Helicobacter pylori (H. pylori) infection has been regarded as an important risk factor of chronic gastritis and peptic ulcer. Eradication of H. pylori can accelerate the healing of peptic ulcer, but whether it can affect the pathologic changes of gastric mucosa needs to be investigated. Aims: To evaluate the effect of eradication of H. pylori on the pathologic changes of gastric mucosa and its precancerous status in patients with chronic gastritis. Methods: Multicentre randomized controlled clinical trial and retrospective cohort study were conducted. All samples were selected from two rural areas of Shanghai, Jinshan and Fengxian districts, with high incidence of gastric cancer. 360 patients endoscopically diagnosed as chronic gastritis and/or duodenal ulcer with H. pylori infection were recruited and randomly divided into two groups. In the treatment group triple therapy (proton pump inhibitor or H2-receptor antagonist plus two antibiotics) was used, and in the control group cisapride was given to patients with chronic gastritis, and cimetidine to patients with duodenal ulcer. All patients were followed-up by endoscopy at the end of 1 and 4 years. Two cohorts were determined basing on the results of positive and negative H. pylori tested histologically. The biopsied specimens of gastric mucosa were reviewed by two pathologists. Results: At the end of 4 years 120 patients were followed up. Among them, 54 patients were H. pylori eradicated and 5 patients were H. pylori positive again, while 45 patients were H. pylori positive and 16 were H. pylori negative. In those who were persistent H. pylori positive, at the end of first year the proportion of active inflammation decreased (P0.05). At the end of fourth year, the degree of chronic inflammation and intestinal metaplasia, as well as the proportion of active inflammation decreased (P0.05). In those H. pylori were persistently positive, the degree of chronic inflammation increased at the end of first year (P0.05), the degree of chronic inflammation, intestinal metaplasia and the proportion of active inflammation increased at the end of fourth year (P0.05). At the end of fourth year the degree of atrophy was more significant than that at the end of first year (P0.05). Conclusions: Eradication of H. pylori can mitigate the degree of chronic gastritis and impede the development and progress of intestinal metaplasia.
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Background: Helicobacter pylori (H. pylori) infection has been regarded as an important risk factor of chronic gastritis and peptic ulcer. Eradication of H. pylori can accelerate the healing of peptic ulcer, but whether it can affect the pathologic changes of gastric mucosa needs to be investigated. Aims: To evaluate the effect of eradication of H. pylori on the pathologic changes of gastric mucosa and its precancerous status in patients with chronic gastritis. Methods: Multicentre randomized controlled clinical trial and retrospective cohort study were conducted. All samples were selected from two rural areas of Shanghai, Jinshan and Fengxian districts, with high incidence of gastric cancer. 360 patients endoscopically diagnosed as chronic gastritis and/or duodenal ulcer with H. pylori infection were recruited and randomly divided into two groups. In the treatment group triple therapy (proton pump inhibitor or H2-receptor antagonist plus two antibiotics) was used, and in the control group cisapride was given to patients with chronic gastritis, and cimetidine to patients with duodenal ulcer. All patients were followed-up by endoscopy at the end of 1 and 4 years. Two cohorts were determined basing on the results of positive and negative H. pylori tested histologically. The biopsied specimens of gastric mucosa were reviewed by two pathologists. Results: At the end of 4 years 120 patients were followed up. Among them, 54 patients were H. pylori eradicated and 5 patients were H. pylori positive again, while 45 patients were H. pylori positive and 16 were H. pylori negative. In those who were persistent H. pylori positive, at the end of first year the proportion of active inflammation decreased (P0.05). At the end of fourth year, the degree of chronic inflammation and intestinal metaplasia, as well as the proportion of active inflammation decreased (P0.05). In those H. pylori were persistently positive, the degree of chronic inflammation increased at the end of first year (P0.05), the degree of chronic inflammation, intestinal metaplasia and the proportion of active inflammation increased at the end of fourth year (P0.05). At the end of fourth year the degree of atrophy was more significant than that at the end of first year (P0.05). Conclusions: Eradication of H. pylori can mitigate the degree of chronic gastritis and impede the development and progress of intestinal metaplasia.
Key concepts: Medicine, Internal medicine, Gastroenterology, Helicobacter pylori, Gastritis, Chronic gastritis, Gastric mucosa, Incidence (geometry)