Document Detail


Rebound acid hypersecretion from a physiological, pathophysiological and clinical viewpoint.
MedLine Citation:
PMID:  20001749     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: The recent description of dyspepsia in healthy individuals after stopping treatment with proton-pump inhibitors (PPIs) indicates that reflux disease may worsen due to this treatment. The aim of this paper is to review current knowledge of the regulation of gastric acid secretion, including maximal acid secretion, and to improve understanding of the pathogenesis of acid-related conditions. MATERIAL AND METHODS: We reviewed our findings from three decades of studies on gastric acid secretion in the isolated rat stomach and in humans as well as studies by the group of Robert Jensen involving gastrinoma patients. RESULTS: The parietal cell has receptors for histamine and acetylcholine, whereas the gastrin receptor is localized to the enterochromaffin-like (ECL) cell. Gastrin-stimulated histamine release depends on the ECL cell mass, which is regulated by gastrin. The parietal cell mass is also influenced by gastrin. All conditions with hypergastrinemia concomitant with a normal oxyntic mucosa result in an increase in acid secretion. Helicobacter pylori infection in the antral mucosa may induce duodenal ulcers by its effect on acid secretion, as in patients with gastrinoma. Whereas PPIs induce clinically important rebound acid hypersecretion, histamine-2 blockers do not, since they also induce tolerance. CONCLUSION: From a biological and physiological point of view, patients should be given treatment that disturbs the normal physiology as little as possible.
Authors:
Helge L Waldum; Gunnar Qvigstad; Reidar Fossmark; Per M Kleveland; Arne K Sandvik
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Scandinavian journal of gastroenterology     Volume:  45     ISSN:  1502-7708     ISO Abbreviation:  Scand. J. Gastroenterol.     Publication Date:  2010 Apr 
Date Detail:
Created Date:  2010-03-22     Completed Date:  2010-07-15     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0060105     Medline TA:  Scand J Gastroenterol     Country:  England    
Other Details:
Languages:  eng     Pagination:  389-94     Citation Subset:  IM    
Affiliation:
Department of Gastroenterology and Liver Diseases, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway. helge.waldum@ntnu.no
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MeSH Terms
Descriptor/Qualifier:
Animals
Dyspepsia / etiology*
Enterochromaffin-like Cells / secretion*
Gastric Acid / secretion*
Gastrinoma / metabolism
Gastroesophageal Reflux / drug therapy*,  metabolism
Helicobacter Infections / metabolism
Helicobacter pylori
Histamine / metabolism
Histamine H2 Antagonists / administration & dosage
Humans
Parietal Cells, Gastric / secretion
Proton Pump Inhibitors / administration & dosage*
Rats
Stomach Neoplasms / metabolism
Chemical
Reg. No./Substance:
0/Histamine H2 Antagonists; 0/Proton Pump Inhibitors; 51-45-6/Histamine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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