| 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 |
Related Documents
:
|
8584419 - Peptide yy release after intraduodenal, intraileal, and intracolonic administration of ... 7864119 - Vitamin a trafficking in caco-2 cells stably transfected with cellular retinol binding ... 6820479 - Induction of wet-dog shakes by intracerebral 'acid' trh in rats. 236059 - Activation of histidine decarboxylase by h2-receptor blockade: mechanism of action. 17080639 - Comparative studies on the effect of a protein-synthesis inhibitor on aluminium-induced... 10888729 - Effects of sodium fluoride on water and acid secretion, soluble mucus and adherent mucu... 6693979 - Leucine, isoleucine and valine requirements of immature beagle dogs. 7469619 - Biologic importance of arachidonic acid. 16545389 - Boric acid inhibits adenosine diphosphate-ribosyl cyclase non-competitively. |
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 |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| 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
Previous Document: Endosonographic elastography of the anal sphincter in patients with fecal incontinence.
Next Document: Outcomes and safety of rapid desensitization for chemotherapy hypersensitivity.