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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
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 to loss of acid secretion is therefore crucial to understanding the pathogenesis of gastric neoplasia.
The effect of H pylori infection on gastric acid secretion depends on the severity and distribution of gastritis. Antral inflammation is associated with increased production of gastrin, which in turn increases the drive for acid secretion by parietal cells in the gastric corpus. If the corpus is affected by severe inflammation, the host’s ability to respond to the increased gastrin is greatly attenuated. Thus subjects with severe corpus inflammation have reduced capacity …
Conflict of interest: None declared.