Histomorphological characteristics of gastric mucosa in patients with Zollinger-Ellison syndrome or autoimmune gastric atrophy: Role of gastrin and atrophying gastritis

The role of gastrin in the pathophysiology of two diseases affecting the hu man stomach, the Zollinger Ellison syndrome (ZES) and the pernicious anemia (PA), is reviewed. Both diseases present chronic hypergastrinemia but from different origins. The ZES is characterized by the occurrence of ectopic e ndocrine gastrin-secreting tumors and PA by a fundic atrophic gastritis lea ding to complete atrophy of fundus and resulting in achlorhydria. In PA, th e lack of acid induces continuous gastrin cell activation and is responsibl e for the subsequent gastrin hypersynthesis and secretion. In ZES, hypergas trinemia causes hypertrophy of the oxyntic mucosa, which, in addition, disp lays hyperplasia of parietal and mucus cells. In both diseases, hypergastri nemia also induces the hyperproliferation of enterochromaffin-like endocrin e cells in the fundic mucosa, which can offer all aspects from hyperplasia, then dysplasia, until true carcinoid tumor. The influence of antisecretory treaments and MEN 1 in the ZES as well as that of several other factors an d antrectomy in PA on the behavior of the different gastric cells is evoked . Finally, the role that gastrin and its receptor play in the maintenance o f the normal development of gastric mucosa and gastric acid secretion is em phasized by results observed in gene knockout models. (C) 2000 Wiley-Liss. Inc.