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enterochromaffin-like cell hyperplasia

Friday 8 February 2013

hyperplasia of enterochromaffin-like cells; gastric endocrine cell hyperplasia; gastric enterochromaffin-like cell hyperplasia

Endocrine cells of the gastric oxyntic mucosa, and especially the enterochromaffin-like cells (ECL), are the progenitors of gastrin-promoted proliferative lesions whose tumorigenic potential largely depends on the background condition in which they arise.

Types

  • diffuse hyperplasia of enterochromaffin-like cells
  • linear hyperplasia of enterochromaffin-like cells
  • micronodular hyperplasia of enterochromaffin-like cells
  • adenomatoid hyperplasia of enterochromaffin-like cells

Enterochromaffin-like cell lesions

The endocrine cell lesions have been classified as:
- pseudohyperplasia : cell clustering unassociated with cell proliferation.
- hyperplasia of enterochromaffin-like cells
- dysplasia of enterochromaffin-like cells

  • enlarged
  • adenomatous or fused micronodules of enterochromaffin-like cells
  • microinfiltration of enterochromaffin-like cells
  • nodular growth of enterochromaffin-like cells

- neoplasia of enterochromaffin-like cells (intramucosal carcinoid tumor or invasive carcinoid tumor).

The entire spectrum of endocrine cell proliferation, from hyperplasia to dysplasia and neoplasia, has been observed in MEN-ZES and diffuse type ACAG.

Both hyperplastic and pseudohyperplastic changes occur with some frequency in the Helicobacter pylori-related chronic gastritis associated with ulcer disease or dyspepsia.

However, because no progression to dysplastic or neoplastic lesions has thus far been documented in these latter conditions, their role in gastric endocrine cell tumorigenesis appears negligible. (#7762735#)

Endocrine cell nodules

Endocrine cell nodules comprised a similar mixture of endocrine cells, sometimes communicating with glands of pseudopyloric metaplasia and proving to be reversible in one case, provides evidence that these nodules are hyperplastic, but finally may lead to gastric carcinoid tumors in AGA.

Size less than 150 micron (0.150 mm), basal location, and mixed hormone content may be helpful criteria for the distinction of hyperplastic endocrine cell nodules from small carcinoid tumors.

Etiology

- hypertrophic gastropathy due to the familial multiple endocrine neoplasia-associated Zollinger-Ellison syndrome ( (MEN1-associated ZES),
- hypertrophic gastropathy due to the sporadic Zollinger-Ellison syndrome (ZES),
- diffuse chronic atrophic gastritis restricted to the corpus-fundus (type autoimmune metaplastic atrophic gastritis or ACAG) or autoimmune metaplastic atrophic gastritis (AMAG), with or without associated pernicious anemia,
- Helicobacter pylori-associated chronic atrophic gastritis (Helicobacter pylori-related multifocal chronic atrophic gastritis)

Reference

- Hyperplastic, dysplastic, and neoplastic enterochromaffin-like-cell proliferations of the gastric mucosa. Classification and histogenesis. Solcia E, Fiocca R, Villani L, Luinetti O, Capella C. Am J Surg Pathol. 1995;19 Suppl 1:S1-7. PMID: #7762735#

- Gastric endocrine cell hyperplasia and carcinoid tumors in atrophic gastritis type A. Müller J, Kirchner T, Müller-Hermelink HK. Am J Surg Pathol. 1987 Dec;11(12):909-17. PMID: #3318512#