COMMENTARY
H pylori
Mechanisms of increased acid secretion after eradication of Helicobacter pylori infection
Correspondence to:
Correspondence to:
Professor E M El-Omar
Department of Medicine and Therapeutics, Aberdeen University, Institute of Medical Sciences, Foresterhill, Aberdeen AB25 2ZD, UK; e.el-omar@abdn.ac.uk
Eradication of Helicobacter pylori infection leads to recovery of gastric acid secretion in some individuals but the mechanism is not fully understood. In the short term, there is an impressive increase in expression of H+/K+-ATPase pumps without an increase in the number of parietal cells. Longer follow up studies are needed to see if the parietal cell mass eventually recovers
Keywords: H+/K+-ATPase; eradication therapy; parietal cell marker; Helicobacter pylori
| The first 150 words of the full text of this article appear below. |
Gastric acid secretion represents an important non-immunological first line of defence against ingested microbes. Almost all vertebrates produce acid in their upper gastrointestinal tracts, suggesting that this physiological process has a fundamental survival advantage. The ability to produce acid allowed vertebrates to ingest more complex diets, but more importantly, it protected them against microbes that gained access through the gastrointestinal tract. It seems that a pH of 4 or less is crucial in protecting the host against ingested bacteria and any therapy or disease that raises the intragastric pH above 4 will allow bacterial overgrowth to occur.1 Perhaps the most important consequence of loss of gastric acid secretion is the increased risk of developing gastric cancer. This complication develops after decades of severe destructive inflammation, and usually in the context of Helicobacter pylori induced chronic gastritis. Understanding the mechanism by which inflammation, H pylori induced or otherwise, leads
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Gut 2006 55: 152-157.[Abstract] [Full Text] [PDF]
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