scholarly journals ABNORMALITIES IN N15 EXCRETION RATES AFTER INGESTION OF TAGGED GLYCINE IN CUSHING'S SYNDROME AND FOLLOWING ACTH ADMINISTRATION 1

1952 ◽  
Vol 31 (6) ◽  
pp. 548-554 ◽  
Author(s):  
William Parson ◽  
K. R. Crispell ◽  
Arthur Ebbert
1986 ◽  
Vol 32 (1) ◽  
pp. 93-96 ◽  
Author(s):  
M Schöneshöfer ◽  
B Weber ◽  
W Oelkers ◽  
K Nahoul ◽  
F Mantero

Abstract To evaluate their potential usefulness in the differential diagnosis of Cushing's syndrome, we estimated the urinary excretion rates of the following non-metabolized, unbound steroid hormones: pregnenolone, progesterone, 17-OH-pregnenolone, 17-OH-progesterone, dehydroepiandrosterone (DHEA), androstenedione, testosterone, dihydrotestosterone, 11-deoxycorticosterone, 11-deoxycortisol, corticosterone, cortisol, 18-OH-11-deoxycorticosterone, 18-OH-corticosterone, and aldosterone. These were measured in normal subjects and in patients with Cushing's disease, adrenal adenoma, or ectopic corticotropin syndrome. We used "high-performance" liquid chromatography and subsequent radioimmunoassay. Our results indicate that simultaneous estimation of urinary free cortisol and DHEA may be useful in differential diagnosis of hypercorticoid states due to adrenal adenoma and Cushing's disease.


1975 ◽  
Vol 48 (2) ◽  
pp. 97-105 ◽  
Author(s):  
C. L. Cope ◽  
S. Loizou

1. Radioimmunoassay has been used to detect and estimate the urinary excretion of deoxycorticosterone (DOC) in normal, hypertensive and hypokalaemic subjects. The range of excretions in ten healthy normal subjects was 41–232 pmol (13.7–76.7 ng) daily, with a mean of 124 pmol (41 ng). 2. In fourteen subjects with essential hypertension without metabolic disturbance the range found was 29–144 pmol (9.7–47.7 ng) daily, with a mean of 87 pmol (28.8 ng), which is not significantly different from that in normal subjects. 3. In twelve patients with Cushing's syndrome due to adrenal cortical hyperplasia the range found was 26–542 pmol (8.7–179 ng). Ten of these twelve patients had values within normal limits. 4. Of nine subjects showing hypokalaemia, eight had elevated excretion of deoxycorticosterone with values from 263 to 5515 pmol (87–1820 ng) daily. Seven of these were hypertensive and two were normotensive. The elevated excretion of deoxycorticosterone found in hypokalaemic subjects is thus not confined to those with hypertension. 5. No correlation has been found between excretion rates for aldosterone and deoxycorticosterone. Raised excretion of the latter provides an indicator of disturbed adrenal cortical metabolism.


1962 ◽  
Vol 24 (2) ◽  
pp. 199-214 ◽  
Author(s):  
C. H. GRAY ◽  
J. M. GREENAWAY ◽  
N. J. HOLNESS ◽  
D. A. SHAW

SUMMARY The metabolism of [4-14C]cortisol in a patient with Cushing's syndrome has been studied by the isolation, identification and measurement of the specific radioactivities of the major metabolites. The results show that the metabolism of cortisol was not abnormal in the aspects studied. The biological half-lives of cortisol and of the tetrahydrocorticosteroid metabolites were found to be normal. Data obtained on excretion rates of metabolites indicated that the metabolic pathways of cortisol were normal. There was no evidence for an increased conversion of cortisol to 6β-hydroxycortisol when the excretion of the latter was expressed as a fraction of the cortisol production. The overall pattern was one of an abnormally high secretion of cortisol by the adrenals, resulting in a proportionally high excretion of tetrahydrocortisone, tetrahydrocortisols, cortolones, cortols, 11-oxygenated 17-oxosteroids, 6β-hydroxycortisol, cortisone and cortisol. Apart from an increased ratio of 11β-hydroxy-metabolites to 11-oxo-metabolites, each metabolite, expressed as a fraction of the cortisol secreted, was excreted in a normal proportion. Hence, in spite of the grossly elevated cortisol secretion rate, the major pathways available for cortisol metabolism were not overloaded and there was no evidence of increased metabolism via minor pathways. Evidence for an increased secretion of corticosterone by the adrenals was obtained by the isolation of abnormal amounts of tetrahydrocorticosterone.


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