Endoscopic, Histological and Serologic Findings of Gastric Hyperplastic Polyps after Eradication of <i>Helicobacter pylori</i>: Comparison between Responder and Non-Responder Cases

Abstract

Background: Evidence indicates that eradication of Helicobacter pylori leads to the disappearance of hyperplastic polyps in the stomach. However, there are some exceptions. We have compared endoscopic and serologic findings of responder and non-responder cases with hyperplastic polyps to try to identify the cause(s), other than H. pylori infection, of the formation or growth of gastric hyperplastic polyps. Methods: We retrospectively studied 33 patients whose hyperplastic polyps disappeared after eradication of H. pylori and 10 patients whose hyperplastic polyps did not disappear after eradication. The patients were examined both endoscopically and serologically before, 1–3 months after and 12–15 months after the eradication. Results: The responder and non-responder groups were similar with respect to age, sex, coexisting diseases, and histologic findings. The number and maximum size of polyps tended to be larger before treatment in the non-responder group than in the responder group. The serum gastrin level was higher in the non-responder group than in the responder group before, 1–3 months after and 12–15 months after the eradication (p = 0.0096, p > 0.2, p = 0.0014). On histologic examination, similar reductions in the degree of inflammatory cell infiltration in the gastric mucosa of the antrum and body were seen in both the responder and non-responder groups. In the non-responders, the size and numbers of the polyps regressed in 5 of the 10 patients. The score of glandular atrophy in the antrum and the serum gastrin levels in the non-regressed cases was higher than those in the regressed cases at 1–3 and 12–15 months after eradication. Conclusion: Persistent high gastrin levels were found in the non-responder cases with gastric hyperplastic polyps.

Predictive findings forHelicobacter pylori-uninfected, -infected and -eradicated gastric mucosa: Validation study

“…Gastric cancer can, however, still occur in eradicated cases, but it is generally difficult to diagnose and few predictive endoscopic findings have been reported. Of those that have been suggested are the disappearance of rugal hyperplasia [8] and hyperplastic polyp [25] , but as these findings need to be compared before and after eradication therapy, on their own it seems difficult to apply them to clinical use. Atrophic change, occurring as a result of H. pylori infection, is thought to remain after eradication therapy [26] .…”

The changing histological pattern of gastric polyps in an ethnically heterogeneous population

“…Infection with H. pylori increases the mucosal injury and inflammation as well as epithelial healing with increase in epithelial cell turnover, and regeneration and the development of hyperplastic tissue that may persist and progress to the development of hyperplastic polyps [25]. Eradication of H. pylori may cause the regression of hyperplastic polyps [26]. Secondary hypergastrinemia may be caused by either chronic infection with H. pylori or chronic exposure to PPI (as reviewed in [25]).…”

“…The indications for EGD expanded [8,9], the proportion of patients receiving proton pump inhibitors (PPIs) increased enormously [10] and the proportion of patients infected with Helicobacter pylori (H. pylori) decreased due to the implementation of eradication therapy (as reviewed in [11]). These changes may influence the occurrence of gastric polyps and the relative prevalence of the hyperplastic polyps and FGPs [2,[12][13][14][15][16][17][18][19]. In a recent study from the USA that included 121,564 patients who underwent EGDs during 1-year period, the prevalence of gastric polyps in the EGD population was 6.35% [15].…”

Serum gastrin levels in different stages of distal gastric carcinogenesis: Is there a role for serum gastrin in tumor growth?

“…However, it is still unclear whether gastrin is a central player or a secondary phenomenon in the development of gastric adenocarcinoma (12). To date, only a few clinical studies have shown that hypergastrinemia is related to gastric hyperplastic polyp (HP), which often regresses after Helicobacter eradication therapy (13)(14)(15).…”