Hypergastrinemia and enterochromaffin-like cell hyperplasia.

UNLABELLED: 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. The most widely accepted nomenclature for the description of hyperplastic proliferation has been retrospectively arranged in a sequence presumed to reflect a temporal evolution of the proliferative process. A comparative, prospective study aimed to verify, in human hypergastrinemic diseases such as atrophic body gastritis (ABG), Zollinger-Ellison syndrome (ZES) and antral gastrin cell hyperfunction (AGCH), the effect of exposure of ECL cells to different pattern of gastrin hypersecretion, is lacking. To this purpose, we studied a series of consecutive patients with ABG, ZES and AGCH at the time of first diagnosis.

MATERIAL AND

METHODS

The patients included in this study (124 ABG, 18 ZES and 10 AGCH) were selected on the basis of two previously performed screening studies aimed to diagnose these diseases. All patients at the time of diagnosis underwent gastroscopy, with multiple biopsies of the gastric body mucosa for the evaluation of qualitative pattern of ECL cells hyperplasia, and basal fasting gastrin determination. A sample of hypergastrinemic patients from each group was further investigated by meal-stimulation of gastrin secretion and quantitative morphometry for CgA positive gastric body endocrine cells.

RESULTS

AGCH patients showed only the normal or simple hyperplasia pattern. In the ZES group, simple and linear grades accounted for 38.4 percent and 46.1 percent, respectively. MEN-I patients showed only these two patterns. The majority of ABG patients showed the presence of micronodular pattern (59.7 percent). A correlation analysis between fasting gastrin levels and grade of hyperplasia (r = 0.5580, p < 0.0001), indicates that the greater the gastrin levels, the higher is the degree of severity of ECL hyperplasia pattern. In conclusion, our data support the role of gastrin as the selective contributor to the progression of ECL cell hyperplasia in humans.