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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
|
pubmed:dateCreated |
1992-2-25
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pubmed:abstractText |
Although Helicobacter pylori is now recognized as playing an etiologic role in chronic gastritis and peptic ulcer disease, information on the pathogenesis and natural history of infection is limited. A model is proposed in which luminal H. pylori secrete substances that mediate inflammation that is beneficial to the organism but ultimately deleterious for the host; in addition to tissue damage, inflammation also affects gastric secretory function. In this model, the host may attempt to suppress the inflammatory response, and the adequacy of this postulated down-regulation determines pathological and clinical outcome. The effects of the inflammatory process on gastrin-hydrochloric acid homeostasis may be of critical importance in the pathogenesis of peptic ulcer disease. Because the long-term consequences of H. pylori colonization reflect the continued presence of the organism in the host over years or decades, it may be useful to consider this as a "slow" bacterial infection.
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pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
AIM
|
pubmed:status |
MEDLINE
|
pubmed:month |
Feb
|
pubmed:issn |
0016-5085
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
102
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
720-7
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading | |
pubmed:year |
1992
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pubmed:articleTitle |
Hypotheses on the pathogenesis and natural history of Helicobacter pylori-induced inflammation.
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pubmed:affiliation |
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Review
|