dc.contributorUNIV CALIF SAN FRANCISCO
dc.contributorUniversidade Federal de São Paulo (UNIFESP)
dc.creatorBiglieri, E. G.
dc.creatorKater, C. E.
dc.date.accessioned2016-01-24T11:40:01Z
dc.date.accessioned2023-09-04T18:26:40Z
dc.date.available2016-01-24T11:40:01Z
dc.date.available2023-09-04T18:26:40Z
dc.date.created2016-01-24T11:40:01Z
dc.date.issued1991-01-01
dc.identifierJournal of Steroid Biochemistry and Molecular Biology. Oxford: Pergamon-Elsevier B.V., v. 40, n. 4-6, p. 493-499, 1991.
dc.identifier0960-0760
dc.identifierhttp://repositorio.unifesp.br/handle/11600/25186
dc.identifier10.1016/0960-0760(91)90268-A
dc.identifierWOS:A1991GT37900002
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8614727
dc.description.abstractWhile hypertension is observed in only two of the three major subtypes of congenital adrenal hyperplasia (CAH), 11-beta- and 17-alpha-hydroxylase deficiencies, deoxycorticosterone (DOC) production is increased in all. the elevated zona fasciculata (ZF) DOC produces mineralocorticoid hypertension with suppressed renin and reduced potassium concentrations. the DOC levels in 21 -hydroxylase deficiency are in part produced by renin stimulation of the Zona glomerulosa (ZG) along with aldosterone. Assessment of the mineralocorticoid hormones of the ZF and ZF (17-deoxy steroids) provides additional unique characteristics of each subtype. Dissociation of DOC from cortisol is not unique to CAH. This dissociation is seen in other disorders and contrived conditions. There is a strong suggestion of a non-ACTH regulator of 17-deoxy steroids (DOC) that may contribute significantly to DOC production in general and effect DOC levels in CAH.
dc.languageeng
dc.publisherElsevier B.V.
dc.relationJournal of Steroid Biochemistry and Molecular Biology
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.rightsAcesso restrito
dc.titleMINERALOCORTICOIDS in CONGENITAL ADRENAL-HYPERPLASIA
dc.typeArtigo


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