What is ECL hyperplasia?

ECL cell hyperplasia is a direct result of elevated gastrin levels, which are elevated in response to the hypochlorhydria of AG. Hypochlorhydria results from loss of oxyntic mucosa and possibly from the disruption of normal parietal cell maturation (12).

What stimulates the ECL cell?

The cells are stimulated by gastrin and pituitary adenylate cyclase activating peptide and suppressed by somatostatin and galanin. Choline esters and histamine seem to be without effect on ECL cell secretion.

What is Enterochromaffin like cell hyperplasia?

The enterochromaffin-like (ECL) cells, the most frequent endocrine cells of the oxyntic mucosa of the stomach, are under the trophic stimulus of gastrin. These cells undergo a hyperplastic increase in variety of hypergastrinemic diseases.

Does somatostatin inhibit ECL cells?

Somatostatin, acting on somatostatin receptor type 2 (SSTR2), interferes with this axis by suppressing the activity of the gastrin cells, ECL cells, and parietal cells.

What causes enterochromaffin cell-like ( ECL ) hyperplasia?

Enterochromaffin cell-like (ECL) hyperplasia is a benign, but potentially pre-neoplastic condition associated with hypergastrinemic states. Hypergastrinemia may be induced by: potent inhibitors of acid secretion (H2-blockers or proton pump inhibitors omeprazole, lansoprazole, pantoprazole);

What kind of tumor is an ECL cell?

Such hypertrophy of ECL cells is particularly evident in patients with gastrin-secreting tumors. ECL-origin tumors, or carcinoids, are commonly found in humans and certain rodents.

When does ECL dysplasia-carcinoid tumor sequence occur?

The ECL hyperplasia – dysplasia – carcinoid tumor sequence occurs in approximately 4% of patients with pernicious anemia-associated chronic atrophic gastritis after an average of 19-year clinical course.

What is the difference between endocrine hyperplasia and neoplasia?

Endocrine cell hyperplasia and neoplasia are equivalent terms to those used below Diagnostic Criteria Gastric carcinoids and neuroendocrine cell proliferations arise in three settings Type A – autoimmune gastritis Hyperplasia, dysplasia and neoplasia are not uncommon Most carcinoids are <1 cm and are not aggressive