Document Detail


Helicobacter pylori, acid and gastrin.
MedLine Citation:
PMID:  7600135     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Before the discovery of Helicobacter pylori, duodenal ulcers were thought to be caused by excessive acid secretion. Duodenal ulcer patients have more parietal cells than controls. In addition, they cannot suppress their acid secretion when the gastric lumen is empty or acidic. These changes, plus an increase in the release of gastrin were attributed to a paucity of the inhibitory peptide somatostatin in the gastric mucosa. It has now been established that the paucity of somatostatin and the failure to suppress acid secretion are actually the result of H. pylori infection. In patients without duodenal ulcers H. pylori infection is often associated with decreased acid secretion. This occurs on first infection and also later because H. pylori gastritis predisposes to gastric atrophy.
Authors:
J Calam
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  European journal of gastroenterology & hepatology     Volume:  7     ISSN:  0954-691X     ISO Abbreviation:  Eur J Gastroenterol Hepatol     Publication Date:  1995 Apr 
Date Detail:
Created Date:  1995-08-07     Completed Date:  1995-08-07     Revised Date:  2009-10-16    
Medline Journal Info:
Nlm Unique ID:  9000874     Medline TA:  Eur J Gastroenterol Hepatol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  310-7     Citation Subset:  IM    
Affiliation:
Department of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London, UK.
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MeSH Terms
Descriptor/Qualifier:
Duodenal Ulcer / metabolism*
Gastric Acid / secretion*
Gastrins / secretion*
Helicobacter Infections / metabolism
Helicobacter pylori / physiology*
Humans
Chemical
Reg. No./Substance:
0/Gastrins

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


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