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      Gastric neuroendocrine tumor with Helicobacter pylori-associated chronic gastritis

      case-report

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          Highlights

          • The increasing number of screening gastroscopies and biopsies have resulted in the frequent detection of ECL tumors.

          • They are regarded as a separate clinicopathological entity seen in the setting of hypergastrinemic states, and their pathogenesis follows the sequence “hyperplasia-dysplasia- neoplasia”.

          • Gastric NETs are divided into two broad categories: gastrin-dependent and non-gastrin dependent or sporadic, which are independent of the trophic effect of gastrin.

          • In view of its aggressive nature and significant mortality, non-gastrin dependent NET should be treated with partial or total gastrectomy.

          Abstract

          Introduction

          Development of gastric neuroendocrine neoplasms in subjects infected with Helicobacter pylori is rare and it occurs through pathogenetic mechanisms related to gastrin.

          Presentation of case

          We report a case of gastric neuroendocrine tumor in a patient infected with Helicobacter pylori and normal gastrin levels. He was treated by endoscopic mucosal dissection after eradication of Helicobacter pylori infection. Histologically the tumor was consistent with a grade 2 well differentiated neuroendocrine tumor. It was characterized by the presence of lymphoid aggregates around and inside the neoplasia.

          Discussion

          Helicobacter pylori-associated chronic gastritis can rarely cause the development of gastric neuroendocrine tumors through mechanisms unrelated to gastrin.

          Conclusion

          The one related to a chronic Helicobacter pylori infection may be considered a distinct type of gastric neuroendocrine tumor.

          Related collections

          Most cited references19

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          The epidemiology of gastroenteropancreatic neuroendocrine tumors.

          In this article, updated analyses of the National Cancer Institute Surveillance, Epidemiology and End Results (SEER) registry (1973-2007) are presented and compared with epidemiologic GEP-NET data from Europe and Asia. Several studies have demonstrated a steadily increasing incidence of GEP-NETs, and this escalation is still ongoing (SEER data 2004-2007). The common primary GEP-NET sites exhibit unique epidemiologic profiles with distinct patterns of incidence, age at diagnosis, stage, and survival. Overall, GEP-NET survival has improved over the past 3 decades, although the outcome for poorly differentiated tumors remains dismal. Copyright © 2011 Elsevier Inc. All rights reserved.
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            Helicobacter pylori-induced gastric pathology: insights from in vivo and ex vivo models

            ABSTRACT Gastric colonization with Helicobacter pylori induces diverse human pathological conditions, including superficial gastritis, peptic ulcer disease, mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric adenocarcinoma and its precursors. The treatment of these conditions often relies on the eradication of H. pylori, an intervention that is increasingly difficult to achieve and that does not prevent disease progression in some contexts. There is, therefore, a pressing need to develop new experimental models of H. pylori-associated gastric pathology to support novel drug development in this field. Here, we review the current status of in vivo and ex vivo models of gastric H. pylori colonization, and of Helicobacter-induced gastric pathology, focusing on models of gastric pathology induced by H. pylori, Helicobacter felis and Helicobacter suis in rodents and large animals. We also discuss the more recent development of gastric organoid cultures from murine and human gastric tissue, as well as from human pluripotent stem cells, and the outcomes of H. pylori infection in these systems.
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              Helicobacter pylori infection and chronic gastric acid hyposecretion.

              We have identified a subgroup of Helicobacter pylori-infected subjects with low or absent gastric acid output. The aim of this study was to document the morphological and functional abnormalities in these subjects and to assess the effect of eradicating the infection. The 16 hypochlorhydric subjects (6 men) had a mean age of 55 years (range, 36-79 years). They underwent a 14C-urea breath test, H. pylori serology, fasting gastrin, gastric autoantibodies, gastroscopy with antral and body biopsies, and measurement of peak acid output to pentagastrin (PAO(PG)). Their histology was compared with that of age- and sex-matched duodenal ulcer and nonulcer dyspepsia patients (16 each). H. pylori infection was eradicated in the hypochlorhydric subjects, and the investigations were repeated 6 months later. Compared with controls, the hypochlorhydric subjects had less dense H. pylori colonization, body-predominant colonization and gastritis, and increased prevalence of body atrophy and intestinal metaplasia. Median PAO(PG) before eradication in the hypochlorhydric subjects was 1.1 mmol/h and increased to 12.6 mmol/h after eradication (P < 0.001), with no significant change in body atrophy or intestinal metaplasia. In some subjects, chronic H. pylori infection produces a body-predominant gastritis and profound suppression of gastric acid secretion that is partially reversible with eradication therapy.
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                Author and article information

                Contributors
                Journal
                Int J Surg Case Rep
                International Journal of Surgery Case Reports
                Elsevier
                2210-2612
                15 September 2020
                2020
                15 September 2020
                : 75
                : 361-366
                Affiliations
                [a ]Unit of Anatomic Pathology, Vito Fazzi Hospital, Lecce, Italy
                [b ]Unit of Digestive Endoscopy, Vito Fazzi Hospital, Lecce, Italy
                Author notes
                [* ]Corresponding author. gserio81@ 123456hotmail.com
                Article
                S2210-2612(20)30754-9
                10.1016/j.ijscr.2020.09.081
                7522572
                32980709
                5865d9e7-b06b-45b7-9d43-cc8d50092e1a

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 27 July 2020
                : 10 September 2020
                : 10 September 2020
                Categories
                Case Report

                gastric neuroendocrine tumor,gastritis,helicobacter pylori

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