Enterochromaffin-like cells and gastric argyrophil carcinoidosis.
The relevance of enterochromaffin-like (ECL) cells in gastric pathobiology has generated considerable interest particularly since the recent description of a pathological state characterized as gastric argyrophilic carcinoidosis. The morphological and biofunctional properties of these cells are distinct from other gastric endocrine cells. It is probable that ECL cells have a major role in the regulation of parietal cell function. Other possible functions may include a trophic regulatory influence. Of particular interest is the recent observation that agents which result in profound and sustained acid inhibition may cause ECL cell hyperplasia. This phenomenon has also been noted in human disease states in which a significant decrease in acid section is evident (pernicious anemia/atrophic gastritis). In patients with gastrinomas of the multiple endocrine neoplasia type I group, therapeutically induced acid inhibition may result in gastric ECL hyperplasia and even neoplasia (gastric carcinoid or ECLoma). Similarly, in the rodent species mastomys, which is genetically predisposed to the formation of gastric carcinoids, exposure to acid inhibitory agents results in rapid (90-120 days) development of gastric carcinoids. The pathobiological relevance of ECL cells and the mechanisms of their inducible hyperplasia and neoplasia may be of considerable significance in understanding the regulatory role of gastric endocrine cells.
Modlin
I M
IM
Department of Surgery, Yale University School of Medicine, New Haven, Connecticut.
Esterline
W
W
Kim
H
H
Goldenring
J R
JR
D000818:Animals; D002276:Carcinoid Tumor / Q000378:metabolism / Q000473:pathology*; D004195:Disease Models, Animal; D004759:Enterochromaffin Cells / Q000737:chemistry / Q000473:pathology*; D006965:Hyperplasia; D009115:Muridae; D051381:Rats; D013270:Stomach / Q000473:pathology*; D013274:Stomach Neoplasms / Q000378:metabolism / Q000473:pathology*