Proposed mechanism of induction of gastric carcinoids: the gastrin hypothesis.

Abstract:

:Novel, powerful and long-acting inhibitors of gastric acid secretion include second generation H2-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 hypergastrinaemia 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.

journal_name

Eur J Clin Invest

authors

Håkanson R,Sundler F

doi

10.1111/j.1365-2362.1990.tb01780.x

subject

Has Abstract

pub_date

1990-10-01 00:00:00

pages

S65-71

eissn

0014-2972

issn

1365-2362

journal_volume

20 Suppl 1

pub_type

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