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Hypergastrinemia and gastric enterochromaffin-like cells.
Am J Surg Pathol. 1995; 19 Suppl 1:S8-19.AJ

Abstract

The enterochromaffin-like (ECL) cell of the oxyntic, acid-secreting mucosa is at present the most extensively studied endocrine cell type in the gastrointestinal tract. It is functionally related to acid secretion through paracrine release of histamine. Its ability to undergo proliferation in response to the trophic stimulus of hypergastrinemia has important implications in pathology, being involved in the development of ECL-cell carcinoid tumors of rodents treated with powerful inhibitors of acid secretion as well as in that of most human gastric carcinoids which, with rare exceptions, are composed of ECL cells. The various aspects of the ECL-cell response to hypergastrinemia in humans are discussed in this review. The trophic effect of gastrin is specific for ECL cells and its sensitivity is enhanced by the female sex and by the genetic background of the multiple endocrine neoplasia type 1 (MEN-1) syndrome. Exposure of ECL cells to hypergastrinemia induces peculiar changes in the structure of cytoplasmic granules and triggers the phenotypic expression of a novel protein, the alpha subunit of glycoprotein hormones, absent in normal cells. The ECL-cell hyperplasia driven by hypergastrinemia may influence the hypersecretory gastric state of patients with Zollinger-Ellison syndrome (ZES) by inappropriate intramucosal secretion of histamine and may contribute to the high circulating levels of basic fibroblast growth factor (bFGF), an ECL-cell product responsible for parathyroid mitogenic effects in MEN-1 patients. However, hypergastrinemia per se cannot promote evolution of hyperplasia into carcinoid tumors, for which additional unknown factors, particularly associated with atrophic gastritis or MEN-1 syndrome, are required. ECL-cell carcinoids developing within these backgrounds have a strikingly more favorable course than their gastrin-independent counterpart. Suppression of hypergastrinemia, either by antrectomy or treatment with somatostatin analogues, may induce regression of both ECL-cell hyperplasia and gastrin-sensitive ECL-cell carcinoids.

Authors+Show Affiliations

Institute of Anatomic Pathology, University of Parma, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

7762739

Citation

Bordi, C, et al. "Hypergastrinemia and Gastric Enterochromaffin-like Cells." The American Journal of Surgical Pathology, vol. 19 Suppl 1, 1995, pp. S8-19.
Bordi C, D'Adda T, Azzoni C, et al. Hypergastrinemia and gastric enterochromaffin-like cells. Am J Surg Pathol. 1995;19 Suppl 1:S8-19.
Bordi, C., D'Adda, T., Azzoni, C., Pilato, F. P., & Caruana, P. (1995). Hypergastrinemia and gastric enterochromaffin-like cells. The American Journal of Surgical Pathology, 19 Suppl 1, S8-19.
Bordi C, et al. Hypergastrinemia and Gastric Enterochromaffin-like Cells. Am J Surg Pathol. 1995;19 Suppl 1:S8-19. PubMed PMID: 7762739.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hypergastrinemia and gastric enterochromaffin-like cells. AU - Bordi,C, AU - D'Adda,T, AU - Azzoni,C, AU - Pilato,F P, AU - Caruana,P, PY - 1995/1/1/pubmed PY - 1995/1/1/medline PY - 1995/1/1/entrez SP - S8 EP - 19 JF - The American journal of surgical pathology JO - Am. J. Surg. Pathol. VL - 19 Suppl 1 N2 - The enterochromaffin-like (ECL) cell of the oxyntic, acid-secreting mucosa is at present the most extensively studied endocrine cell type in the gastrointestinal tract. It is functionally related to acid secretion through paracrine release of histamine. Its ability to undergo proliferation in response to the trophic stimulus of hypergastrinemia has important implications in pathology, being involved in the development of ECL-cell carcinoid tumors of rodents treated with powerful inhibitors of acid secretion as well as in that of most human gastric carcinoids which, with rare exceptions, are composed of ECL cells. The various aspects of the ECL-cell response to hypergastrinemia in humans are discussed in this review. The trophic effect of gastrin is specific for ECL cells and its sensitivity is enhanced by the female sex and by the genetic background of the multiple endocrine neoplasia type 1 (MEN-1) syndrome. Exposure of ECL cells to hypergastrinemia induces peculiar changes in the structure of cytoplasmic granules and triggers the phenotypic expression of a novel protein, the alpha subunit of glycoprotein hormones, absent in normal cells. The ECL-cell hyperplasia driven by hypergastrinemia may influence the hypersecretory gastric state of patients with Zollinger-Ellison syndrome (ZES) by inappropriate intramucosal secretion of histamine and may contribute to the high circulating levels of basic fibroblast growth factor (bFGF), an ECL-cell product responsible for parathyroid mitogenic effects in MEN-1 patients. However, hypergastrinemia per se cannot promote evolution of hyperplasia into carcinoid tumors, for which additional unknown factors, particularly associated with atrophic gastritis or MEN-1 syndrome, are required. ECL-cell carcinoids developing within these backgrounds have a strikingly more favorable course than their gastrin-independent counterpart. Suppression of hypergastrinemia, either by antrectomy or treatment with somatostatin analogues, may induce regression of both ECL-cell hyperplasia and gastrin-sensitive ECL-cell carcinoids. SN - 0147-5185 UR - https://www.unboundmedicine.com/medline/citation/7762739/Hypergastrinemia_and_gastric_enterochromaffin_like_cells_ DB - PRIME DP - Unbound Medicine ER -