Abstract
It is now well established that Helicobacter pylori is the major acquired factor in the pathogenesis of duodenal ulcer (DU) disease. The infection is found in > 95% of DU patients and numerous studies have demonstrated that eradicating the infection markedly lowers the ulcer relapse rate1–5. The mechanism by which the infection predisposes to ulceration of the duodenum has been the subject of much speculation. The fact that the infection is most pronounced in the stomach, whereas the associated ulceration occurs in the duodenum, suggests that the ulceration is not merely due to local damage of the mucosa by the organism. The antrum plays an important role in the regulation of gastric acid secretion via the release of the hormone gastrin. One hypothesis linking H. pylori infection and duodenal ulceration is that the infection stimulates an increased release of gastrin, which in turn produces increased acid secretion, and that the excessive duodenal acid load causes the ulceration6.
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McColl, K.E.L., El-Omar, E. (1994). Effect of H. pylori infection on gastrin and gastric acid secretion. In: Hunt, R.H., Tytgat, G.N.J. (eds) Helicobacter pylori. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-1418-9_21
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DOI: https://doi.org/10.1007/978-94-011-1418-9_21
Publisher Name: Springer, Dordrecht
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