CHEMICAL METHOD FOR THE DETERMINATION OF 17-Hydroxycorticosteroids AND 17-Ketosteroids IN URINE FOLLOWING HYDROLYSIS WITH Β-Glucuronidase*

Glenn, E. Myles; Nelson, Don H.

doi:10.1210/jcem-13-8-911

Cited by 245 publications

(20 citation statements)

References 12 publications

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“…However, the percentage of stimulation varied from one case to another. The stimulation was normal in cases 3-5, 9, and 13, low but significant in cases 1, 2, 6-8, 11, and 12, and undetectable in case 10.…”

Section: Resultsmentioning

confidence: 83%

ACTH and prostaglandin receptors in human adrenocortical tumors. Apparent modification of a specific component of the ACTH-binding site.

Saez¹,

Dazord²,

Gallet³

1975

J. Clin. Invest.

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A B S T R A C T The failure of certain adrenal tumors to respond to ACTH was investigated in vivo by administration of corticotropin-( 1-24) -tetracosapeptide (ACTH1-2) and dexamethasone and in vitro by studying the binding properties of ACTH1-2 and prostaglandin E1 (PGE1) and their effect on adenylate cyclase activity of the tumors' crude membranes; in addition, in five cases the stimulation of cortisol production in isolated adrenal cells by both hormones and dibutyryl cyclic adenosine 3',5'-monophosphate (cAMP) was also studied. The results obtained in 13 hormone-producing tumors of the human adrenal cortex, i.e. 10 carcinomas and 3 adenomas, were compared with those found in normal human adrenal glands.According to the adenylate cyclase responses to ACTH1-and PGE1, the tumors fall into different categories. In the first group are six tumors in which the adenylate cyclase was stimulated by both ACTHl-2X and PGE1; in addition specific binding could be demonstrated for the two hormones in all six. The binding affinity for 'I-ACTH1-2 was found to be about 10 times higher than that for 'I-ACTHu-24. In the one tumor in which the experiment was performed, bound 'I-ACTH1-X was displaced by ACTH1-1o. These results are similar to the ones found in normal human adrenal preparations. For two tumors of the group in which ACTH did not increase steroidogenesis in vivo, the biochemical abnormality might be located beyond cAMP formation.A preliminary report of this work was presented at the 55th Meeting of the Endocrine

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Section: Resultsmentioning

confidence: 83%

ACTH and prostaglandin receptors in human adrenocortical tumors. Apparent modification of a specific component of the ACTH-binding site.

Saez¹,

Dazord²,

Gallet³

1975

J. Clin. Invest.

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“…Total urinary 17-ketosteroids (17-KS) were measured by a modification of the method of CALLOW et al [7] and 17-hydroxycorticosteroids (17-OHCS) by a modification [14] of the method of GLENN and NELSON [9].…”

Section: Methodsmentioning

confidence: 99%

The Syndrome of Congenital Adrenocortical Unresponsiveness to ACTH. Report of Six Cases

et al. 1968

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Six patients with the syndrome of congenital adrenocortical unresponsiveness to ACTH are reported. This syndrome is characterized by feeding problems early in life, hypoglycemic episodes and hyperpigmentation of the skin (table I). Blood pressure and levels of electrolytes in serum were normal (table II). PPD and histoplasmin skin tests were negative, while antibodies to adrenal, thyroid, and gastric tissues were undetectable. Urinary excretion of 17-hydroxycorticosteroids and cortisol production rates were low and did not respond to administration of ACTH (table III). While receiving a low sodium diet, the patients were able to conserve sodium (figs. 2, 3 and 4) and to increase the rate of aldosterone secretion (tables IV and V).In one case, adrenal pathology showed a normal zona glomerulosa with atrophy of the zonae fasciculata and reticularis.This isolated deficiency in cortisol secretion is not due to a defect in pituitary function or a deficiency of one of the enzymes directly involved in steroid biosynthesis. The most probable pathogenesis is an abnormality at the site (or one of the sites) of ACTH action on cortisol biosynthesis. Speculation

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“…Samples of each fraction were taken for counting of C14. After removing the sample from fraction six, the residual extract was evaporated to dryness and subsequent chromatography performed on a Florisil column to separate the 17-KS and the tetrahydro compounds with 4%o and 25%o concentrations of methanol in chloroform, respectively (20). The column eluates were evaporated, made up to volume with methanol, and samples taken for counting C14.…”

Section: Methodsmentioning

confidence: 99%

Effect of Diphenylhydantoin on Cortisol Metabolism in Man *

Werk¹,

MacGee²,

Sholiton³

1964

J. Clin. Invest.

166

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During a study of cortisol metabolism in advanced cancer and other disease states (1), we observed in patients receiving DPH 1 therapy for convulsive seizures an abnormal pattern of excretion of cortisol metabolites in urine. This abnormal pattern was characterized by increased urinary output of the polar unconjugated metabolite 6-OHF, suggesting an interference with extraadrenal metabolism of cortisol by DPH. We =5,5'-diphenylhydantoin; 6-hydroxycortisol (6 -OHF) = 6a (/3), 11,/, 17a, 21 -tetrahydroxy -4 -pregnene-3,20 -dione; 17-OHCS = 17-hydroxycorticosteroids; ACTH = adrenocorticotrophic hormone; methopyrapone (Metopirone, Ciba Pharmaceutical Co., Summit, N. J.) =2-methyl-1,2-di-(3-pyridyl)-1-propanone. Tetrahydro derivatives: THF (tetrahydrocortisol) = 3a,11,, 17a,21-tetrahydroxy-5/8-pregnan-20-one; allo-THF (allotetrahydrocortisol) = 3a,11/3,17a,21-tetrahydroxy-5a-?pregnan-20-one; THE (tetrahydrocortisone) = 3a,17a,21-trihydroxy-5p-pregnan-11,20-dione. Cortol = 3a,11,8,17a,20a (/3),21-pentahydroxy-5/3-pregnane; cortolone = 3a,17a,20a (/3) ,21-tetrahydroxy-5/8-pregnan-11-one; 17-KS = 17-ketosteroids; 1 1-hydroxyetiocholanolone = 3a,1j1/-dihydroxy-5,B-androstan-17-one; dehydroisoandrosterone = 3/3-hydroxy-5-androstene-17-one; TPNH = reduced triphosphopyridine nucleotide; o,p'DDD = 2,2-bis (2-chlorophenyl,4-chlorophenyl) 1,1-dichloroethane. since a) adrenal hypertrophy was observed in intact rats and b) in adrenalectomized rats treated with DPH a more profound decrease in brain excitability was demonstrated than in intact rats. Goncharov has observed that acute administration of DPH to dogs and guinea pigs increases adrenocortical output of cortisol (3). Reports by Staple (4) and Bonnycastle and Bradley (5) have, however, indicated an inhibition of pituitary-adrenal secretion after chronic DPH treatment of mice and rats.In humans also cortisol has been shown to enhance brain excitability (6). After chronic DPH therapy to patients, excretion of corticosteroids in urine is reported to decrease (7, 8) after an initial increase (7). These findings have led to the suggestion that the decrease in brain excitability induced by DPH might be mediated partially through adrenocortical suppression. However, levels of 17-OHCS in plasma from patients treated with DPH are usually normal (8, 9), as are responses to ACTH (8, 9) and rates of disappearance from plasma of infused cortisol (8). These observations detract from the possibility that direct adrenocortical suppression plays a significant role in therapeutic effectiveness of DPH. Recently, however, Krieger has demonstrated that control subjects treated with DPH manifest a reduced response in the methopyrapone test, which suggests an interference with ACTH release (10).2) The increased excretion of 6-OHF produced by DPH appears to be similar to that we have observed in patients with advanced cancer and certain terminal illnesses (1) as well as to that reported after estrogen therapy (11), during pregnancy (12), and in newborn infants (13).Thus we hoped that furthe...

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CHEMICAL METHOD FOR THE DETERMINATION OF 17-Hydroxycorticosteroids AND 17-Ketosteroids IN URINE FOLLOWING HYDROLYSIS WITH Β-Glucuronidase*

Cited by 245 publications

References 12 publications

ACTH and prostaglandin receptors in human adrenocortical tumors. Apparent modification of a specific component of the ACTH-binding site.

ACTH and prostaglandin receptors in human adrenocortical tumors. Apparent modification of a specific component of the ACTH-binding site.

The Syndrome of Congenital Adrenocortical Unresponsiveness to ACTH. Report of Six Cases

Effect of Diphenylhydantoin on Cortisol Metabolism in Man *

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