Linked Life Data

7372059

Source:http://linkedlifedata.com/resource/pubmed/id/7372059

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1980-7-12
pubmed:abstractText
Lithocholate, a secondary bile acid, is hepatotoxic in many animal species including nonhuman primates. The induced histologic changes resemble those observed in patients with hepatic damage associated with inflammatory bowel disease. Accordingly, we have examined the hypothesis that lithocholate is of etiologic importance in causing this association by measuring serum and biliary lithocholates in inflammatory bowel disease patients with and without liver disease. Serum and biliary lithocholates and isolithocholates were normal in all patients. Because defective sulfation in the nonhuman primate which allows lithocholate to accumulate in the enterohepatic circulation is thought to be responsible for inducing liver damage and because secondary bile acids are reduced after colectomy and in established liver disease, we examined thae capacity of all patients to sulfate labeled lithocholate. Effective sulfation of lithocholate was demstrated in all groups. Despite the hepatotoxic effects observed in nonhuman primates, we have found no evidence so far to implicate lithocholate as an etiologic factor in inflammatory bowel disease and hepatic dysfunction nor have we detected other potentially hepatotoxic bile acids in these patients.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0016-5085
pubmed:author
pubmed:issnType
Print
pubmed:volume
78
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1393-401
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1980
pubmed:articleTitle
Hepatotoxic effect of bile acids in inflammatory bowel disease.
pubmed:publicationType
Journal Article