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      Well-Differentiated Gastric Tumors/Carcinomas

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          Most cited references 18

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          Gastric carcinoids and neuroendocrine carcinomas: pathogenesis, pathology, and behavior.

           S Rappel,  M Stolte,  C Bordi (1996)
          The goal of this study was to provide information of prognostic value for gastric endocrine tumors. A total of 205 gastric endocrine tumors have been studied: 193 well differentiated tumors [2 gastrin cell tumors, 191 enterochromaffin-like (ECL) cell tumors] and 12 poorly differentiated carcinomas. Subtyping of ECL cell tumors (carcinoids) resulted in 152 associated with chronic atrophic gastritis (CAG) (type 1); 12 associated with hypertrophic gastropathy (HG) due to Zollinger-Ellison syndrome with multiple endocrine neoplasia type I (type 2), and 27 with no specific association (type 3, sporadic). Type 1 cases occurred most often in female (108 of 152), elderly (mean 63 years) patients, with no tumor-related death at an overall mean follow-up of 53 months. The 12 type 2 cases were equally distributed between the sexes (six of each), with a mean age of 45 years; there was one tumor-related death (49 months after diagnosis) and an overall mean survival of 84 months. Type 3 cases were mostly in men (20 of 27), with a mean age of 55 years; there were seven tumor-related deaths at a mean follow-up of 28 months. Poorly differentiated neuroendocrine carcinomas were observed in elderly patients (mean 63 years, range 41-76 years) of both sexes, with nine tumor-related deaths and a mean survival of 7 months. It was concluded that correct clinicopathologic subtyping may predict the clinical behavior of gastric endocrine tumors.
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            Treatment of type II gastric carcinoid tumors with somatostatin analogues.

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              Atrophic body gastritis patients with enterochromaffin-like cell dysplasia are at increased risk for the development of type I gastric carcinoid.

              In the presence of atrophic body gastritis, gastric carcinoid develops from gastric-body mucosa enterochromaffin-like cells. Few data exist on the prevalence of enterochromaffin-like dysplastic lesions in atrophic body gastritis patients and their presumed risk of evolution to carcinoid has never been assessed prospectively in humans. The aim of the present study was to investigate the prevalence and incidence of dysplastic and neoplastic enterochromaffin-like cell lesions in a consecutive series of patients with atrophic body gastritis. A total of 130 atrophic body gastritis patients at diagnosis and 96 atrophic body gastritis patients at follow-up (median 30 months) underwent gastroscopy with multiple biopsies and fasting gastrinaemia evaluation. In patients with enterochromaffin-like cell dysplasia, a more detailed bioptic sampling at follow-up was performed. Of the 130 atrophic body gastritis patients, only one (0.7%) had a gastric carcinoid polyp, whereas enterochromaffin-like cell dysplasia was found in five patients (3.8%). At follow-up only one out of the 96 atrophic body gastritis patients (1%) was diagnosed as having a carcinoid polyp at 41 months. Enterochromaffin-like cell dysplasia was present in four additional patients (4.2%). Two atrophic body gastritis pernicious anaemia patients with enterochromaffin-like cell dysplasia developed a gastric carcinoid in the follow-up. Among nine atrophic body gastritis patients with enterochromaffin-like cell dysplasia, the incidence of carcinoid tumour was 22% compared to 1.1% of atrophic body gastritis patients without dysplasia (odds ratio: 26.00; 95% confidence interval: 2.089-323.52). During the follow-up, fasting gastrin levels increased significantly only in atrophic body gastritis patients with enterochromaffin-like cell dysplasia (mean 677.4 +/- 66.1 vs 1112.2 +/- 185.6; P = 0.0287). This study provides the first clinical evidence that, in hypergastrinaemic atrophic body gastritis patients, enterochromaffin-like cell dysplasia carries a markedly increased risk for development of type I gastric carcinoid. This suggests that a more detailed endoscopic/bioptic procedure in this subgroup of atrophic body gastritis patients is able to detect gastric carcinoid at an early stage.

                Author and article information

                S. Karger AG
                February 2007
                23 February 2007
                : 84
                : 3
                : 158-164
                aDepartment of Gastroenterology, Beaujon Hospital, Clichy, France; bDepartment of Digestive and Liver Disease, Ospedale S. Andrea, Rome, Italy; cDepartment of Hepatology and Gastroenterology, CHU Bichat – B. Claude Bernard University, Paris, France; dDepartment of Pathology, Kantonsspital Baden, Switzerland; eDepartment of Gastroenterology, Massachussetts General Hospital, Boston, Mass., USA; fB. Kos-Kudła, Department of Endocrinology, Slaska University, Zabrze, Poland; gDepartment of Surgery, UFR Bichat-Beaujon-Louis Mourier Hospital, Colombes, France; hDepartment of Oncology, Royal Free University, London, UK; iDepartment of Gastroenterology, Philipps University, Marburg, Germany; jDepartment of Surgery, Gothenburg University, Gothenburg, Sweden; kDepartment of Nuclear Medicine, Catholique de Louvain University, Brussels, Belgium; lDepartment of Nuclear Medicine, Erasmus MC University, Rotterdam, The Netherlands; mDepartment of Pathology and Laboratory Medicine, Università degli Studi, Parma, Italy
                98007 Neuroendocrinology 2006;84:158–164
                © 2006 S. Karger AG, Basel

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                Figures: 1, Tables: 2, References: 41, Pages: 7
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