Pathophysiology of duodenal and gastric ulcer and gastric cancerBMJ 2001; 323 doi: https://doi.org/10.1136/bmj.323.7319.980 (Published 27 October 2001) Cite this as: BMJ 2001;323:980
- John Calam,
- J H Baron
Duodenal and gastric ulcers and gastric cancer are common and serious diseases but occur in only a minority of people infected with Helicobacter pylori. Mass eradication of H pylori is impractical because of the cost and the danger of generating antibiotic resistance, so we need to know how to target prophylaxis. Knowledge of the mechanisms that lead to ulcer formation or to gastric cancer in the presence of H pylori infection is therefore valuable.
Various factors affect the outcome of H pylori infection, including the host response and particularly the extent and severity of gastric inflammation and thus the amount of acid secreted by parietal cells. H pylori can elevate acid secretion in people who develop duodenal ulcers, decrease acid through gastric atrophy in those who develop gastric ulcers or cancer, and leave acid secretion largely unchanged in those who do not develop these diseases.
Regulation of gastric acid secretion
Several specialised cells in the gastric mucosa contribute to the control of acid secretion. G cells in the gastric antrum release the hormone gastrin. Gastrin acts on the enterochromaffin-like cells in the gastric corpus to release histamine, which stimulates parietal cells to secrete acid. Gastrin also stimulates parietal cells directly and promotes growth of enterochromaffin-like and parietal cells.
Histamine H2 receptor antagonists act by blocking the effect of histamine on parietal cells. Proton pump inhibitors act by inhibiting the enzyme in parietal cells that catalyses acid production for release into the gastric lumen. G …
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