H.pylori gastric adenocarcinoma pathophysiology
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Gastric cancer is the second leading cause of cancer-related deaths worldwide and H. pylori is the strongest known risk factor for gastric cancer. H. pylori is considered as type I carcinogen. Among infected individuals, 1 to 3% develop gastric adenocarcinoma.
- Gastric cancer is the second leading cause of cancer-related deaths worldwide and H. pylori is the strongest known risk factor for gastric cancer.
- H. pylori is considered as type I carcinogen. Among infected individuals, 1 to 3% develop gastric adenocarcinoma.
- Patients with H. pylori infection with severe atrophic gastritis, corpus predominant gastritis, or both and Intestinal metaplasia are at increased risk for intestinal-type gastric carcinoma.
- Gastric cancer is caused by H. pylori infection either by inflammatory process or by its direct effect on gastric mucosa.
- H. pylori releases phospholipases, ammonia and cytotoxins directly into gastric lumen and causes epithelial degeneration.
- Following epithelial damage, there will be persistent proliferation and regeneration of gastric epithelial cells. This increases the risk of malignant alterations (metaplastic changes) of the gastric stem cells at the neck of gastric tubes.
- The nitric oxide (NO) and reactive oxygen metabolites are released by [[neutrophils] during the inflammatory process, which contribute to the DNA damage of epithelial cells.
- The above process along with deficiency of ascorbic acid(vitamin C) , vitamin E and calcium leads to epithelial cell DNA damage.
- Diet containing high amount of salt, nitrates or nitrosamines also contribute to the DNA damage leading to gastric cancer.
- Patients with duodenal ulcer have predominant antral gastritis where as gastric cancer patients have severe gastritis predominantly in the corpus of the stomach.
- Severe gastritis in corpus leads to decreased acid production resulting in suppression of a defense mechanism against atypical cell production (atypical cells are very sensitive to gastric acid) leading to persistence and progression of atypical cells.
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