Highlights & Basics
- Achlorhydria indicates the inability to produce gastric acid. This is most commonly caused by gastric atrophy. Gastric atrophy, with or without autoimmune gastritis, is present in about 15% of older people and is thought to be initiated by infection with Helicobacter pylori.
- Patients are usually asymptomatic but may present with signs and/or symptoms of iron, cobalamin (vitamin B12), or calcium deficiency and may predispose to enteric infection with organisms such as Clostridium difficile, Salmonella, and Campylobacter.
- Achlorhydria may interfere with the absorption of certain drugs including thyroxine, ketoconazole, itraconazole, and dipyridamole.
- The physiologic response to achlorhydria/gastric atrophy is hypergastrinemia. This is the most common cause of hypergastrinemia.
- Although the prognosis is excellent, it carries a small increased risk for the development of gastric adenocarcinoma and gastric carcinoid tumor.
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Model illustrating physiologic regulation of gastric acid secretion by gastrin, histamine, somatostatin (SST), and luminal acid. Gastrin, released from antral G cells, is the main hormonal stimulant of acid secretion during meal ingestion. Gastrin acts directly on the acid-secreting parietal cells and, more importantly, indirectly by stimulating histamine secretion from enterochromaffin-like (ECL) cells. Histamine diffuses to adjacent parietal cells, where it binds to histamine H2 receptors coupled to stimulation of acid secretion. In the interdigestive phase, somatostatin (SST), released from antral D cells in response to luminal acid, tonically inhibits gastrin secretion from G cells, thereby maintaining acid secretion at an economically low level.
Model illustrating pathophysiology of achlorhydria and the development of gastric carcinoid tumors. With achlorhydria, the stimulatory effect of luminal acid on SST is lost. Consequently, SST secretion is decreased and its inhibitory restraint on gastrin secretion attenuated (disinhibition), resulting in hypergastrinemia. Gastrin is not only a secretagogue but also a trophic hormone that induces growth of the oxyntic mucosa. If hypergastrinemia is sustained for days, ECL cells will hypertrophy; if sustained for weeks to months, ECL cells become hyperplastic, dysplastic, and, in some patients, become carcinoid tumors.
Classification of gastric carcinoid tumors
Citations
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