In atrophic gastritis or partial gastrectomy, in patients with a long history of H. pylori infection, as
well as in patients on long-term anti-acid therapy, insufficient pepsin or gastric secretion and
inadequate proteolytic digestion there is a failure to dissociate cobalamin from food, thus preventing
its absorption [11–13]. Moreover, inadequate functional gastric mucosa, gastrectomy, gastric bypass
and atrophic gastritis lead to IF deficiency, which, in turn, causes insufficient cobalamin absorption.
However, only 30% of patients undergoing partial gastrectomy will eventually have cobalamin
malabsorption, and an even smaller proportion will develop frank clinical manifestation of cobalamin
deficiency, such as megaloblastic anemia.
In atrophic gastritis or partial gastrectomy, in patients with a long history of H. pylori infection, aswell as in patients on long-term anti-acid therapy, insufficient pepsin or gastric secretion andinadequate proteolytic digestion there is a failure to dissociate cobalamin from food, thus preventingits absorption [11–13]. Moreover, inadequate functional gastric mucosa, gastrectomy, gastric bypassand atrophic gastritis lead to IF deficiency, which, in turn, causes insufficient cobalamin absorption.However, only 30% of patients undergoing partial gastrectomy will eventually have cobalaminmalabsorption, and an even smaller proportion will develop frank clinical manifestation of cobalamindeficiency, such as megaloblastic anemia.
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