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QUANTITATIVE ESTIMATION OF ADRENOCORTICAL HORMONES AND THEIR α-KETOLIC METABOLITES IN URINE

QUANTITATIVE ESTIMATION OF ADRENOCORTICAL HORMONES AND THEIR α-KETOLIC METABOLITES IN URINE ABSTRACTUrinary corticosteroid patterns were estimated in patients with hyperadrenocorticism including Cushing's syndrome, adrenogenital syndrome and Conn's syndrome.The patterns reflect excessive hormone production, undue secretion of precursors and altered metabolism of cortisol (F) and corticosterone (B) in such a characteristic way that differential diagnosis is considerably facilitated.In Cushing's disease (bilateral adrenocortical hyperplasia) the patterns indicate a hypersecretion of cortisol and its immediate precursor Reichstein's S. All other hormones and precursors are produced in essentially normal amounts. The metabolic pathway of cortisol and corticosterone is shifted in favour of tetrahydrocortisol (THF) and tetrahydrocorticosterone (THB) respectively, at the cost of allotetrahydrocortisol (allo-THF) and tetrahydrocortisone (THE), allotetrahydrocorticosterone (allo-THB) and tetrahydro-11-dehydrocorticosterone (THA) respectively.In adrenocortical carcinoma the undue loss of precursors (Reichstein's S and possibly 17-hydroxyprogesterone) seems to be an essential feature, irrespective whether cortisol or androgens are produced in abnormally large amounts. The excretion of tetrahydro-11-deoxycortisol (THS) particularly may be used to differentiate between adrenal hyperplasia and carcinoma.In adrenogenital syndrome (congenital adrenal hyperplasia due to defective 21-hydroxylation) the patterns, in combination with the values for groupwise estimated total 17-hydroxycorticosteroids, reflect an excessive secretion of 17-hydroxyprogesterone. The production of corticosterone is very low, presumably because continuous ACTH stimulation of the adrenals favours the synthesis of 17-hydroxysteroids (high F/B-ratio).In Conn's syndrome the patterns reflect a rather low secretion of cortisol and a low F/B-ratio in addition to the absolutely or relatively increased secretion of aldosterone. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png European Journal of Endocrinology Oxford University Press

QUANTITATIVE ESTIMATION OF ADRENOCORTICAL HORMONES AND THEIR α-KETOLIC METABOLITES IN URINE

Cost, W. S.; Pol, J.
European Journal of Endocrinology , Volume 42 (1): 14 – Jan 1, 1963
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Copyright
© Published by Oxford University Press.
ISSN
0804-4643
eISSN
1479-683X
DOI
10.1530/acta.0.0420039
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Abstract

ABSTRACTUrinary corticosteroid patterns were estimated in patients with hyperadrenocorticism including Cushing's syndrome, adrenogenital syndrome and Conn's syndrome.The patterns reflect excessive hormone production, undue secretion of precursors and altered metabolism of cortisol (F) and corticosterone (B) in such a characteristic way that differential diagnosis is considerably facilitated.In Cushing's disease (bilateral adrenocortical hyperplasia) the patterns indicate a hypersecretion of cortisol and its immediate precursor Reichstein's S. All other hormones and precursors are produced in essentially normal amounts. The metabolic pathway of cortisol and corticosterone is shifted in favour of tetrahydrocortisol (THF) and tetrahydrocorticosterone (THB) respectively, at the cost of allotetrahydrocortisol (allo-THF) and tetrahydrocortisone (THE), allotetrahydrocorticosterone (allo-THB) and tetrahydro-11-dehydrocorticosterone (THA) respectively.In adrenocortical carcinoma the undue loss of precursors (Reichstein's S and possibly 17-hydroxyprogesterone) seems to be an essential feature, irrespective whether cortisol or androgens are produced in abnormally large amounts. The excretion of tetrahydro-11-deoxycortisol (THS) particularly may be used to differentiate between adrenal hyperplasia and carcinoma.In adrenogenital syndrome (congenital adrenal hyperplasia due to defective 21-hydroxylation) the patterns, in combination with the values for groupwise estimated total 17-hydroxycorticosteroids, reflect an excessive secretion of 17-hydroxyprogesterone. The production of corticosterone is very low, presumably because continuous ACTH stimulation of the adrenals favours the synthesis of 17-hydroxysteroids (high F/B-ratio).In Conn's syndrome the patterns reflect a rather low secretion of cortisol and a low F/B-ratio in addition to the absolutely or relatively increased secretion of aldosterone.

Journal

European Journal of Endocrinology – Oxford University Press

Published: Jan 1, 1963

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