Linked Life Data

7440699

Source:http://linkedlifedata.com/resource/pubmed/id/7440699

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1981-2-19
pubmed:abstractText
A search was made for an abnormality in aldosterone biosynthesis in congenital adrenal hyperplasia due to a cortisol 21-hydroxylation defect. Examination of the urinary metabolites of potential C-18-oxygenated steroid precursors revealed an abnormal pattern; however, the locus of the defect was not at the C-21 hydroxylation step, but consisted of overproduction of glomerulosa 18-hydroxylation step, but consisted of overproduction of glomerulus 18-hydroxycorticosterone relative to aldosterone, as seen in the type II corticosterone methyl oxidase defect. This abnormality, which was seen in all salt losers and most nonsalt losers, provided evidence for diminished aldosterone secretory reserve even when values of the hormone are normal or elevated. These findings support the concept that salt-losing and nonsalt-losing forms of the cortisol 21-hydroxylation defect differ only in degree and are not different genotypes. An implication of these findings is that all patients with congenital adrenal hyperplasia with an elevated 18-hydroxycorticosterone to aldosterone metabolite ratio should be considered for mineralocorticoid replacement therapy even if their absolute aldosterone values appear to be normal or elevated.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0021-972X
pubmed:author
pubmed:issnType
Print
pubmed:volume
51
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1346-53
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1980
pubmed:articleTitle
Evidence for an aldosterone biosynthetic defect in congenital adrenal hyperplasia.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.