Abstract
We report a child in whom DOC excess secondary to congenital adrenal hyperplasia (CAH, 11 beta-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 glomerulosa of the adrenal cortex under the independent control of the ACTH and renin-angiotensin systems respectively.
Publication types
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Case Reports
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Research Support, Non-U.S. Gov't
MeSH terms
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Adrenal Cortex / metabolism*
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Adrenal Hyperplasia, Congenital* / complications*
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Adrenal Hyperplasia, Congenital* / drug therapy
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Adrenal Hyperplasia, Congenital* / metabolism
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Child
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Desoxycorticosterone / metabolism*
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Dexamethasone / therapeutic use
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Drug Therapy, Combination
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Fludrocortisone / therapeutic use
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Humans
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Hypertension, Malignant / drug therapy
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Hypertension, Malignant / etiology*
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Male
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Renin / metabolism*
Substances
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Desoxycorticosterone
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Dexamethasone
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Renin
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Fludrocortisone