Linked Life Data

6618108

Source:http://linkedlifedata.com/resource/pubmed/id/6618108

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1983-11-23
pubmed:abstractText
In order to characterize the mechanism(s) causing vitamin E deficiency during chronic childhood cholestasis, we studied 6 vitamin E-deficient cholestatic children with clinical evidence of neurologic dysfunction (group A), 4 vitamin E-sufficient cholestatic children and young adults with normal neurologic status (group B), and 6 vitamin E-sufficient noncholestatic children (group C). Intestinal absorption of dl-alpha-tocopherol (assessed by an oral tolerance test) was markedly impaired (p less than 0.001) in group A compared with groups B and C, which did not differ from each other. Intraluminal total bile acid concentrations were markedly depressed in group A compared with age-matched controls (0.50 vs. 7.00 mM, p less than 0.001), whereas concentrations were low normal in group B. Intramuscular dl-alpha-tocopherol was well absorbed in 4 group A subjects and corrected abnormal hydrogen peroxide hemolysis. Our data suggest that low intraluminal bile acid concentrations result in malabsorption and deficiency of vitamin E in children with prolonged, severe cholestasis. Intact plasma transport and tissue uptake of vitamin E during cholestasis suggest that intramuscular vitamin E should be utilized for prevention and therapy of the neurologic abnormalities caused by vitamin E deficiency.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0016-5085
pubmed:author
pubmed:issnType
Print
pubmed:volume
85
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1172-82
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1983
pubmed:articleTitle
Mechanism causing vitamin E deficiency during chronic childhood cholestasis.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't