1996, pp 108-121

Effects of abnormalities of gastrin and somatostatin in Helicobacter pylori infection on acid secretion

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Abstract

Before the discovery of H. pylori the aetiology of gastroduodenal diseases was largely viewed in terms of associated abnormalities of gastric secretion. Elevated acid secretion in patients with duodenal ulcers (DU) seemed likely to be damaging the duodenum, and diminished acid secretion in patients with gastric cancer allowed overgrowth of mitogen-producing bacteria. Consequently gastric cancer and DU rarely occurred in the same patient. Since it emerged that H. pylori plays a major role in these diseases, we and others have investigated the effect of this infection on gastric physiology. Initial work examined how H. pylori might elevate acid secretion in DU disease. As the link between H. pylori and gastric cancer emerged the acid-lowering effects of this infection became more interesting. One part of the work has explored patterns of acid secretion under specific conditions in the different patient groups. Other studies have used in-vitro systems to explore the cellular events which might underlie what is found in patients. We are learning how infection and inflammation affect endocrine and exocrine systems of the gastrointestinal tract. Knowledge remains rudimentary, and whilst we learn more about the effects of relevant factors on various cells it will become necessary to dissect which of these effects actually determine disease outcomes. Hopefully, knowledge of why H. pylori exerts opposite effects on acid in different individuals will help us to identify patients at particular risk of DU or cancer.