PMID- 7762739
OWN - NLM
STAT- MEDLINE
DCOM- 19950623
LR  - 20220409
IS  - 0147-5185 (Print)
IS  - 0147-5185 (Linking)
VI  - 19 Suppl 1
DP  - 1995
TI  - Hypergastrinemia and gastric enterochromaffin-like cells.
PG  - S8-19
AB  - 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.
FAU - Bordi, C
AU  - Bordi C
AD  - Institute of Anatomic Pathology, University of Parma, Italy.
FAU - D'Adda, T
AU  - D'Adda T
FAU - Azzoni, C
AU  - Azzoni C
FAU - Pilato, F P
AU  - Pilato FP
FAU - Caruana, P
AU  - Caruana P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - United States
TA  - Am J Surg Pathol
JT  - The American journal of surgical pathology
JID - 7707904
RN  - 0 (Gastrins)
SB  - IM
MH  - Carcinoid Tumor/pathology
MH  - Enterochromaffin Cells/*pathology/physiology
MH  - Gastric Mucosa/*pathology
MH  - Gastrins/*blood
MH  - Gastritis, Atrophic/pathology
MH  - Humans
MH  - Hyperplasia/pathology
MH  - Stomach Neoplasms/pathology
MH  - Zollinger-Ellison Syndrome/pathology
RF  - 64
EDAT- 1995/01/01 00:00
MHDA- 1995/01/01 00:01
CRDT- 1995/01/01 00:00
PHST- 1995/01/01 00:00 [pubmed]
PHST- 1995/01/01 00:01 [medline]
PHST- 1995/01/01 00:00 [entrez]
PST - ppublish
SO  - Am J Surg Pathol. 1995;19 Suppl 1:S8-19.