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Gastric enterochromaffin‐like cell changes in multiple endocrine neoplasia type 1
Author(s) -
Manoharan Jerena,
Anlauf Martin,
Albers Max B.,
Denzer Ulrike W.,
Mintziras Ioannis,
Wächter Sabine,
Di Fazio Pietro,
Bollmann Carmen,
Bartsch Detlef K.
Publication year - 2021
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/cen.14430
Subject(s) - men1 , chromogranin a , multiple endocrine neoplasia , gastrin , enterochromaffin like cell , medicine , zollinger ellison syndrome , gastrinoma , gastroenterology , endocrinology , enterochromaffin cell , hyperplasia , neuroendocrine tumors , pathology , endocrine system , immunohistochemistry , biology , hormone , receptor , biochemistry , secretion , serotonin , gene
Background Gastric enterochromaffin‐like cell (ECL) tumours can occur in patients with multiple endocrine neoplasia type 1 (MEN1), especially in those affected by Zollinger Ellison syndrome (ZES). Since the prevalence of ECL lesions is not well defined yet, the present study evaluated the presence and extent of ECL lesions in MEN1 patients with and without ZES. Methods Multiple endocrine neoplasia type 1 patients being part of a regular screening program (2014–2018) underwent gastroduodenoscopies with biopsies of the stomach and determination of serum gastrin and chromogranin A levels. Haematoxylin‐ and immunostaining with chromogranin A, gastrin and VMAT I and II (vesicular monoamine transporter I and II) of the biopsies were performed. Results Thirty‐eight MEN1 patients, of whom 16 (42%) were diagnosed and treated earlier for ZES, were analysed. In ten of 16 (62.5%) ZES patients, a locally scattered, mixed image of diffuse, linear and micronodular mild hyperplasia was present. In addition, two of these patients (13%) showed small (max 1.5 mm in size) intramucosal ECL tumours. Neither ECL changes, nor tumours were found in MEN1 patients without ZES ( n = 22). In MEN1/ZES patients, the median serum gastrin level was significantly elevated compared to MEN1 patients without ZES (206 pg/ml vs. 30.5 pg/ml, p < .001). A subgroup analysis of the serum gastrin and chromogranin A levels of MEN1/ZES patients with or without ECL hyperplasia did not show significant differences (gastrin level: p = .302, chromogranin A: p = .464). Conclusion Enterochromaffin‐like cell hyperplasia and gastric carcinoids occur only in MEN1 patients with ZES, but less frequently than reported.