Urinary 18-hydroxycortisol and its relationship to the excretion of other adrenal steroids

C. E. Gomez-Sanchez, R. J. Upcavage, P. G. Zager, M. F. Foecking, O. B. Holland, A. Ganguly

Research output: Contribution to journalArticle

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Abstract

The urinary excretion of 18-hydroxycortisol was recently reported to be increased in patients with primary aldosteronism who have an adrenal adenoma and in those with glucocorticoid-suppressible aldosteronism. A direct RIA for 18-hydroxycortisol in urine and plasma has been described, and we here report our experience using a similar direct RIA and a more elaborate RIA which includes a preliminary high pressure liquid chromatography (HPLC) purification step. The urinary excretion of 18-hydroxycortisol was compared with that of other adrencorticoids. The urinary excretion of 18-hydroxycortisol in 37 normal subjects using the direct RIA was 112 ± 49 (±SD) μg/24 h, and that with the HPLC-RIA method was 63 ± 36 μg/24 h. The accuracy and specificity of the HPLC-RIA assay method were confirmed by measuring the steroid after the HPLC step as the glycolic acid ester derivative. The urinary excretion of 18-hydroxycortisol correlated with that of cortisol (r = 0.36; P < 0.01), 18-oxocortisol (r = 0.42; P < 0.01), and 19-nordeoxycortisosterone (r = 0.71; P < 0.001), but did not correlate with the excretion of aldosterone 18-oxoglucuronide (r = 0.25; P = 0.15942). Dexamethasone administration to five normal subjects significantly decreased 18-hydroxycortisol excretion from 81 ± 47 to 23 ± 8 μg/24 h. ACTH infusion in these subjects receiving dexamethasone significantly raised 18-hydroxycortisol excretion to 147 ± 37 μg/24 h. Five days of a sodium-restricted diet (10 mmoles/day) resulted in a significant (P < 0.02) increase in 18-hydroxycortisol excretion, but two of eight subjects had decreased excretion, although urinary aldosterone excretion increased, as expected. These studies demonstrate that the direct RIA significantly overestimates urinary 18-hydroxycortisol excretion. These studies also demonstrate that the major factor resulting 18-hydroxycortisol excretion is ACTH. However, since 18-hydroxycortisol excretion may increase during sodium depletion, angiotensin or other factors may also regulate its secretion.

Original languageEnglish (US)
Pages (from-to)310-314
Number of pages5
JournalJournal of Clinical Endocrinology and Metabolism
Volume65
Issue number2
StatePublished - 1987

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Steroids
High pressure liquid chromatography
High Pressure Liquid Chromatography
Hyperaldosteronism
glycolic acid
Aldosterone
Adrenocorticotropic Hormone
Dexamethasone
18-hydroxycortisol
Sodium
Sodium-Restricted Diet
Angiotensins
Nutrition
Adenoma
Glucocorticoids
Purification
Hydrocortisone
Assays
Esters
Urine

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology, Diabetes and Metabolism

Cite this

Gomez-Sanchez, C. E., Upcavage, R. J., Zager, P. G., Foecking, M. F., Holland, O. B., & Ganguly, A. (1987). Urinary 18-hydroxycortisol and its relationship to the excretion of other adrenal steroids. Journal of Clinical Endocrinology and Metabolism, 65(2), 310-314.

Urinary 18-hydroxycortisol and its relationship to the excretion of other adrenal steroids. / Gomez-Sanchez, C. E.; Upcavage, R. J.; Zager, P. G.; Foecking, M. F.; Holland, O. B.; Ganguly, A.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 65, No. 2, 1987, p. 310-314.

Research output: Contribution to journalArticle

Gomez-Sanchez, CE, Upcavage, RJ, Zager, PG, Foecking, MF, Holland, OB & Ganguly, A 1987, 'Urinary 18-hydroxycortisol and its relationship to the excretion of other adrenal steroids', Journal of Clinical Endocrinology and Metabolism, vol. 65, no. 2, pp. 310-314.
Gomez-Sanchez CE, Upcavage RJ, Zager PG, Foecking MF, Holland OB, Ganguly A. Urinary 18-hydroxycortisol and its relationship to the excretion of other adrenal steroids. Journal of Clinical Endocrinology and Metabolism. 1987;65(2):310-314.
Gomez-Sanchez, C. E. ; Upcavage, R. J. ; Zager, P. G. ; Foecking, M. F. ; Holland, O. B. ; Ganguly, A. / Urinary 18-hydroxycortisol and its relationship to the excretion of other adrenal steroids. In: Journal of Clinical Endocrinology and Metabolism. 1987 ; Vol. 65, No. 2. pp. 310-314.
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AU - Gomez-Sanchez, C. E.

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N2 - The urinary excretion of 18-hydroxycortisol was recently reported to be increased in patients with primary aldosteronism who have an adrenal adenoma and in those with glucocorticoid-suppressible aldosteronism. A direct RIA for 18-hydroxycortisol in urine and plasma has been described, and we here report our experience using a similar direct RIA and a more elaborate RIA which includes a preliminary high pressure liquid chromatography (HPLC) purification step. The urinary excretion of 18-hydroxycortisol was compared with that of other adrencorticoids. The urinary excretion of 18-hydroxycortisol in 37 normal subjects using the direct RIA was 112 ± 49 (±SD) μg/24 h, and that with the HPLC-RIA method was 63 ± 36 μg/24 h. The accuracy and specificity of the HPLC-RIA assay method were confirmed by measuring the steroid after the HPLC step as the glycolic acid ester derivative. The urinary excretion of 18-hydroxycortisol correlated with that of cortisol (r = 0.36; P < 0.01), 18-oxocortisol (r = 0.42; P < 0.01), and 19-nordeoxycortisosterone (r = 0.71; P < 0.001), but did not correlate with the excretion of aldosterone 18-oxoglucuronide (r = 0.25; P = 0.15942). Dexamethasone administration to five normal subjects significantly decreased 18-hydroxycortisol excretion from 81 ± 47 to 23 ± 8 μg/24 h. ACTH infusion in these subjects receiving dexamethasone significantly raised 18-hydroxycortisol excretion to 147 ± 37 μg/24 h. Five days of a sodium-restricted diet (10 mmoles/day) resulted in a significant (P < 0.02) increase in 18-hydroxycortisol excretion, but two of eight subjects had decreased excretion, although urinary aldosterone excretion increased, as expected. These studies demonstrate that the direct RIA significantly overestimates urinary 18-hydroxycortisol excretion. These studies also demonstrate that the major factor resulting 18-hydroxycortisol excretion is ACTH. However, since 18-hydroxycortisol excretion may increase during sodium depletion, angiotensin or other factors may also regulate its secretion.

AB - The urinary excretion of 18-hydroxycortisol was recently reported to be increased in patients with primary aldosteronism who have an adrenal adenoma and in those with glucocorticoid-suppressible aldosteronism. A direct RIA for 18-hydroxycortisol in urine and plasma has been described, and we here report our experience using a similar direct RIA and a more elaborate RIA which includes a preliminary high pressure liquid chromatography (HPLC) purification step. The urinary excretion of 18-hydroxycortisol was compared with that of other adrencorticoids. The urinary excretion of 18-hydroxycortisol in 37 normal subjects using the direct RIA was 112 ± 49 (±SD) μg/24 h, and that with the HPLC-RIA method was 63 ± 36 μg/24 h. The accuracy and specificity of the HPLC-RIA assay method were confirmed by measuring the steroid after the HPLC step as the glycolic acid ester derivative. The urinary excretion of 18-hydroxycortisol correlated with that of cortisol (r = 0.36; P < 0.01), 18-oxocortisol (r = 0.42; P < 0.01), and 19-nordeoxycortisosterone (r = 0.71; P < 0.001), but did not correlate with the excretion of aldosterone 18-oxoglucuronide (r = 0.25; P = 0.15942). Dexamethasone administration to five normal subjects significantly decreased 18-hydroxycortisol excretion from 81 ± 47 to 23 ± 8 μg/24 h. ACTH infusion in these subjects receiving dexamethasone significantly raised 18-hydroxycortisol excretion to 147 ± 37 μg/24 h. Five days of a sodium-restricted diet (10 mmoles/day) resulted in a significant (P < 0.02) increase in 18-hydroxycortisol excretion, but two of eight subjects had decreased excretion, although urinary aldosterone excretion increased, as expected. These studies demonstrate that the direct RIA significantly overestimates urinary 18-hydroxycortisol excretion. These studies also demonstrate that the major factor resulting 18-hydroxycortisol excretion is ACTH. However, since 18-hydroxycortisol excretion may increase during sodium depletion, angiotensin or other factors may also regulate its secretion.

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