Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions |
umls-concept:C0001128,
umls-concept:C0014869,
umls-concept:C0030685,
umls-concept:C0030909,
umls-concept:C0035647,
umls-concept:C0035820,
umls-concept:C0040688,
umls-concept:C0391871,
umls-concept:C0680255,
umls-concept:C0699493,
umls-concept:C1283071,
umls-concept:C1521828,
umls-concept:C1527148,
umls-concept:C1963578
|
pubmed:issue |
4
|
pubmed:dateCreated |
1997-4-4
|
pubmed:abstractText |
The impact of intraluminal acid and pepsin on the rate of esophageal luminal release of transforming growth factor alpha (TGF alpha), measured by RIA, in 21 asymptomatic volunteers and 26 patients with reflux esophagitis (RE) was investigated. Esophageal secretion was collected, using an esophageal perfusion catheter, during mucosal exposure to NaCl, HCl or HCl/Pepsin and final saline. The basal rate of luminal TGF alpha release in controls was steady throughout the entire four perfusion periods with saline. This rate declined by 71% during mucosal exposure to HCl (p = 0.002) and by 74% during esophageal perfusion with HCl/pepsin (p = 0.011). The basal rate of luminal TGF alpha release in patients with RE was 27% higher than the corresponding value in controls (1.076 +/- 0.140 vs. 0.850 +/- 0.180 ng/min, p = 0.050). Mucosal exposure to acid and acid/pepsin solutions in RE patients also resulted in a significant decline in the luminal release of TGF alpha by 43% (p < 0.001) and by 42% (p < 0.001) respectively. Despite this decline, TGF alpha in patients with RE was significantly higher (p < 0.001) than in controls. The decline in esophageal TGF alpha release during HCl and HCl/pepsin exposure may facilitate the development of mucosal damage. The increase in esophageal TGF alpha release in patients with RE may represent a compensatory mechanism developed by the mucosal inflammatory changes.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Dec
|
pubmed:issn |
0192-0790
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
23
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
261-8
|
pubmed:dateRevised |
2006-11-15
|
pubmed:meshHeading |
pubmed-meshheading:8957727-Adult,
pubmed-meshheading:8957727-Basal Metabolism,
pubmed-meshheading:8957727-Esophagitis, Peptic,
pubmed-meshheading:8957727-Esophagus,
pubmed-meshheading:8957727-Female,
pubmed-meshheading:8957727-Gastric Acid,
pubmed-meshheading:8957727-Humans,
pubmed-meshheading:8957727-Hydrochloric Acid,
pubmed-meshheading:8957727-Male,
pubmed-meshheading:8957727-Middle Aged,
pubmed-meshheading:8957727-Mucous Membrane,
pubmed-meshheading:8957727-Pepsin A,
pubmed-meshheading:8957727-Transforming Growth Factor alpha
|
pubmed:year |
1996
|
pubmed:articleTitle |
Detrimental impact of acid and pepsin on the rate of luminal release of transforming growth factor alpha. Its potential pathogenetic role in the development of reflux esophagitis.
|
pubmed:affiliation |
University of Virginia Health Sciences Center, Charlottesville 22908, USA.
|
pubmed:publicationType |
Journal Article,
Clinical Trial,
Controlled Clinical Trial,
Research Support, Non-U.S. Gov't
|