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Proposed mechanism of induction of gastric carcinoids: the gastrin hypothesis
Author(s) -
HÅKANSON R.,
SUNDLER F.
Publication year - 1990
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1990.tb01780.x
Subject(s) - enterochromaffin like cell , gastrin , gastric acid , zollinger ellison syndrome , enteroendocrine cell , medicine , omeprazole , hyperplasia , endocrinology , stomach , secretion , proton pump inhibitor , blockade , gastrinoma , gastric mucosa , endocrine system , biology , receptor , hormone
. Novel, powerful and long‐acting inhibitors of gastric acid secretion include second generation H 2 ‐blockers and so‐called proton pump inhibitors, such as omeprazole. Gastric carcinoids were found to develop in experimental animals as a consequence of continuous long‐term administration of several of these highly effective anti secretory drugs. This unwanted side effect is now thought to reflect the fact (1) that pharmacological blockade of acid secretion results in hypergastrinaemia, and (2) that long‐standing hyper‐gastrinaemia gives rise to hyperplasia of certain endocrine cells, the so‐called ECL cells, in the gastric mucosa. The carcinoids that develop in the rat stomach after lifelong treatment with antisecretagogues arise from the ECL cells. The proposed sequence of events is acid blockade—hypergastrinaemia—ECL cell hyperplasia—carcinoid. This concept, referred to as the gastrin hypothesis, maintains that the ECL cell hyperplasia (and possibly the carcinoids) is a consequence of long‐term continuous hypergastrinaemia.