Gastric carcinoid tumors, endocrine cell hyperplasia, and associated intestinal metaplasia. Histologic, histochemical, and immunohistochemical findings.

Eleven cases of gastric carcinoid tumor have been studied to review their clinical and pathologic spectrum, to identify any relationship to pernicious anemia, and to evaluate the accompanying gastric mucosal changes, with particular reference to the endocrine cell population. Seven patients were male and four female; ages ranged from 26 to 83 years. Two male patients had documented pernicious anemia and one female patient had unconfirmed pernicious anemia. All patients had marked gastric intestinal metaplasia (atrophic gastritis), which was predominantly fundal (Type A) in three patients with suspected/proven pernicious anemia and antral (Type B) in the other eight. In seven patients, the tumors were typical carcinoids, whereas in 4 patients the carcinoids were "atypical"; one carcinoid was completely polypoid. All cases were argyrophilic, and focal mucin positivity was present in four. Focal somatostatin immunoreactivity was present in four cases, serotonin in three cases, vasoactive intestinal polypeptide (VIP) in two cases, and gastrin (G) in one case. Endocrine cell hyperplasia was identified in the gastric mucosa of eight of 11 patients, including all cases with pernicious anemia; in three of eight cases, G-cell hyperplasia was evident. Numbers of serotonin-positive cells were increased in areas of intestinal metaplasia in all cases. In two patients, there was marked endocrine-cell hyperplasia with multiple small carcinoid tumorlets; the tumorlets stained for G in one. Gastric intestinal metaplasia includes intestinal-like endocrine cells. An association exists between atrophic gastritis and gastric carcinoids, and there is a histogenetic link between atrophic gastritis and some cases of gastric carcinoid tumor.