Omeprazole, a proton pump inhibitor (PPI) is now widely used for severe erosive esophagitis in both adults and children. Long-term omeprazole treatment is associated with increased levels of serum gastrin (hypergastrinemia) and gastric mucosal change, including parietal cell hypertrophy, an increased number of antral G cells and an increased number of argyrophil cells.
Pashankar and Israel found gastric nodules or polyps in seven of 31 children receiving omeprazole for more than 6 months.57 At histology, nodules, ranging from 2 to 4 mm, showed only mucosal edema and disappeared spontaneously during treatment, whereas gastric polyps, of hyperplastic or fundic gland types, persisted during ongoing therapy. Two different patho-genetic mechanisms for polyp formation have been suggested: it has been proposed that glandular obstructions and dilatation may be caused by increased viscosity of gland secretion, because of decreased gastric acid and fluid output; it has also been speculated that hypertrophy of parietal cells, induced by omeprazole therapy, may increase outflow resistance and induce dilatation of the gland.
This gastropathy seems to be benign, but a careful endoscopic follow-up is suggested in children receiving long-term omeprazole therapy.
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