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Deoxycorticosterone, 11 β‐hydroxylase and the adrenal cortex
Author(s) -
Spoudeas Helen A.,
Slater J. D. H.,
Rumsby Gillian,
Honour John W.,
Brook Charles G. D.
Publication year - 1993
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1993.tb01782.x
Subject(s) - endocrinology , medicine , adrenal cortex , biology
Summary We report a child in whom DOC excess secondary to congenital adrenal hyperplasia (CAH, 11β‐hydroxylase deficiency) caused malignant hypertension. Clinical and metabolic control could be achieved only by replacement of both glucocorticoid and mineralocorticoid, thus confirming in clinical practice the hypothesis that DOC is produced from both the zonae fasciculata and glomeru‐losa of the adrenal cortex under the independent control of the ACTH and renin‐angiotensin systems respectively.