Immunohistochemical Investigation of Gastrin-producing Cells (G Cells)

Abstract

The mucosal distribution of G cells was quantitatively mapped in resected stomachs from 42 patients (12 with gastric ulcer, 11 with duodenal ulcer, 14 with duodenal ulcer and uremia, and 5 with gastric cancer). Along the histological border of the proximal part of the pyloric antrum there was in all patient categories a transitional zone of varying extent, with a low G-cell density before the cells disappeared in the body of the stomach. The proximal end of the duodenum contained considerably fewer G cells than in the antrum, and the number was virtually equal in all groups. Within the antrum there was in the material as a whole a gradual increase in G-cell density from the proximal to the distal part, but this difference was not apparent for the gastric ulcer patients. When corresponding antral segments were compared between the various patient groups, the G-cell density was found to be significantly decreased in the distal antrum of the gastric ulcer patients. In all patient categories, except the duodenal ulcer group with uremia, the circumferential distribution of G cells showed reduced density along the curvatura minor. For the material as a whole there were great individual variations in the overall antral G-cell density, in the antral area corresponding to the distribution of G cells and in the total G-cell mass; these three variables were not significantly related to diagnosis, age or sex.

A histological study of the effect of chronic gastritis on gastrin cell distribution in the human stomach.

“…Apart from this we failed to find gastrin cells within histologically normal fundal mucosa. This is in agreement with the findings of Stave andBrandtzaeg (1976) andHelmstaedter et al (1977). In the presence of pseudopyloric metaplasia within the fundus we consistently found small numbers of immunoreactive gastrin cells within the metaplastic mucosa.…”

“…This supports the findings of Asnaes et al (1976), who investigated antral mucosal biopsies and found an inverse correlation between gastrin cells and the degree of gastritis. Recently, While the above reports and the present study indicate reduced antial gastrin cells in gastritis, neither Meikle et al (1976) nor Fung et al (1977) X.4 Several authors have commented on the marked variation in gastrin cell concentration from one area of the stomach to another noted on studies on gastrectomy specimens (Delaney et al, 1978;Keuppens et al, 1978;Stave and Brandtzaeg, 1976). Similar var-ations have been reported in mucosal biopsies by Bussolati (1970), Creutzfeldt et al (1976), and Asnaes and Johansen (1975).…”

“…This variation can be explained partly by the differing gastrin cell concentration reported within the normal antrum. Stave and Brandtzaeg (1976) noted increasing numbers of gastrin cells in the distal as opposed to the proximal antrum in patients with duodenal ulceration. Keuppens et al (1978) did not confirm this but reported significantly more cells in sections taken from the greater curvature of the antrum than from the lesser curvature.…”

Autoimmune Gastritis: Distinct Histological and Immunohistochemical Findings Before Complete Loss of Oxyntic Glands

“…Nodular hyperplasia was diagnosed when nodular aggregates of at least five chromogranin-positive cells were seen. In the human stomach, gastrin cells are absent from the body mucosa (4,5), and gastrin immunostains were performed in 33 available cases to ensure that the biopsied tissue was from the body.…”

“…Therefore, this study was undertaken to evaluate the diagnosis of AG on endoscopic biopsy specimens of body mucosa that still had oxyntic glands. We also employed immunostains for gastrin (a negative stain indicates that the biopsy specimen is truly from the body and not from the antrum or antral-oxyntic transitional zone (4,5)) and chromogranin to evaluate for ECL cell hyperplasia.…”