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Rebound Hypersecretion after Inhibition of Gastric Acid Secretion
Author(s) -
Qvigstad Gunnar,
Waldum Helge
Publication year - 2004
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2004.pto940502.x
Subject(s) - secretion , histamine , gastric acid , gastrin , enterochromaffin like cell , parietal cell , enterochromaffin cell , medicine , endocrinology , receptor , chemistry , serotonin
Drugs inhibiting gastric acid secretion are widely used because of the high prevalence of acid‐related disorders. However, from clinical experience it seems that symptom relapse is common after withdrawal of these drugs. Experimental as well as clinical studies have demonstrated an increased acid secretion after a period of treatment with either histamine 2 receptor antagonists or proton pump inhibitors. Rebound hypersecretion is likely to reflect the following sequence of events: Long‐term inhibition of acid output is accompanied by elevated serum gastrin levels, leading to enterochromaffin‐like cell activation and proliferation, resulting in increased amounts of histamine being mobilized from these cells to stimulate the parietal cells. The clinical consequences of rebound hypersecretion have not been settled.