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OESO©2011
 
Volume: The Esophagogastric Junction
Chapter: Particular problems in medical therapy
 

Is there any explanation for fundic polyps developing after long-term proton pump inhibitor therapy?

F. Baldi, M.L. Brancaccio, R. Cappiello (Bologna)

After the first report of Graham in 1992 [1] other authors described the possibility of development of gastric polypoid lesions in patients undergoing long-term PPI treatment (Table I) [2-4].

These reports have raised the following questions.
Table I. Gastric fundic polyps after long-term P

Are these polypoid lesions characterized by specific histological features?

The polyps developed after long-term PPI therapy are described as fundic gland polyps and seem to be very similar to the gastric glandular cysts of the oxyntic mucosa, firstly reported by Elster in 1977 [5]. The histological studies performed [2-4] have shown that they consist of mucosal cysts, developing preferentially in oxyntic mucosa, and lined by a mix of mucus, parietal and chief cells. The only difference that has been found, in comparison with the Elster's cysts, is the location in mucosal area showing parietal cell hyperplasia and increased thickness of the parietal cell zone [4]. Thus, it has not yet been clearly established if the polyps developing after long-term PPI therapy should be classified in a different category in comparison with the sporadic fundic gland polyps.

Are these polypoid lesions related to the presence of chronic gastritis
or to the presence of Helicobacter pylori infection?

Literature data have shown that long-term PPI therapy may be associated with the development of chronic atrophic gastritis. Moreover it has been recently suggested [6] that the simultaneous presence in these patients of an Helicobacter pylori infection may promote the development of gastric atrophy. However, the studies performed on patients with gastric polyps after PPI therapy had not shown the presence of Helicobacter pylori associated gastritis. The majority of observations indicate that these fundic polyps develop in normal or hyperplastic oxyntic mucosa.

What is the pathogenesis of these fundic polyps
and does their presence have some clinical implications?

Available data suggest that the development of fundic polyps after long-term PPI treatment is related to a functional-secretory impairment of gastric mucosa, due to the drug administration. In particular it has been suggested that the PPI treatment may induce an accumulation of mucus in the foveola which, due the viscosity of the secretion in the glands ( PPI drugs inhibit acid secretion but do not modify the chief cells and mucus cells secretions ) can lead to a relative obstruction with a formation of retention cysts.

The glandular polyps (Elster's polyps) represent the most frequent gastric polyps detected in patients submitted to endoscopy ( 60% of all the polyps reported in a recent casistic) [7]. They seem to be harmless for the patients, since they do not develop into tumours and because they are very rarely associated with Helicobacter pylori infection [3]. As regards their association with the PPI therapy, the majority of data suggest only a coincidental occurrence without a causal link. On the other hand, despite the fact that many millions of patients have been treated with omeprazole, the development of fundic polyps has been reported only in very few cases.

 

In conclusion, as far as we know, the gastric polyps occasionally developing after a long term PPI therapy do not represent a clinical problem and do not require further diagnostic or therapeutic measures.

References

1. Graham JR. Gastric polyposis: onset during long-term therapy with the omeprazole. Med J Austr 1992;157:287-288.

2. Weinstein WM, et al. Fundic gland polyps in patients on long-term omeprazole therapy: a light and electron microscopic study of the gastric mucosa. Gastroenterology 1994;106:A 210.

3. Stolte M, et al. Omeprazole induced pseudohypertrophy of gastric parietal cells. Z Gastoenterol 1992;30:134-138.

4. Hirt M, et al. Fundic gland polyps: a comparison of the omeprazole-associated and the sporadic types. DDW 1996;A134.

5. Elster K, et al. Drusenkorperzysten, eine polypoide Lasion der Magenscheleimhaut. Dtsch Med Wschr 1977; 6:183-187.

6. Kuipers EJ, et al. Atrophic gastritis and Helicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication. N. Engl J Med1996;334/16:1018-1022.

7. Hirt M, et al. The rapidly changing prevalence of fundic gland polyps (FGP). DDW 1996;A710.


Publication date: May 1998 OESO©2011