PubMed · 6962529
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R Ottenjann. 1982. Mucosal function in gastritis.. https://pubmed.ncbi.nlm.nih.gov/6962529/
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New concepts in the pathophysiology of peptic ulcers must acknowledge 1. the close association of ulcers and Helicobacter pylori infection, 2. the protective role of endogenous prostaglandins, 3. the scarcity of new data on the importance of acidity (though presence of gastric acid remains indispensible for ulcer development). The different pathophysiologically relevant factors closely interact with each other. However, many not of actual concepts are still experimental and--apart from Helicobacter pylori--have not yet led to new therapeutical approaches.
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The implications of profound and sustained suppression of acid secretion are of increasing concern. Short-term inhibition of acid secretion by H2-receptor blockade or proton pump inhibition alters the gastric luminal flora and increases the risk of nosocomial pneumonia in critically ill patients who are receiving prophylaxis for stress gastritis. Long-term suppression alters gut flora, carcinogen levels in the gastric lumen, and the hormonal milieu, leading to proliferative changes in the fundic mucosa. Previous reports have noted a significant incidence of gastric malignancies in the achlorhydric environment of atrophic gastritis and pernicious anemia. Concern has also been expressed regarding the possibility of gastric neoplasia that arises after vagotomy and distal gastrectomy. The exact risk of gastric epithelial and endocrine hyperplasia or neoplasia in patients receiving potent antisecretory agents is not yet known, but such risks cannot be dismissed until long-term follow-up studies are available. The relationship between sustained suppression of acid secretion and the proliferation of epithelial and endocrine elements may provide insight into processes that regulate replication and growth of cells in the gastric mucosa.