FLUCTUABILITY OF STEROID EXCRETION

1957 ◽  
Vol 26 (1) ◽  
pp. 91-95 ◽  
Author(s):  
Herman Zondek ◽  
Gerda W. Zondek ◽  
Hannah E. Leszynsky
Keyword(s):  
1963 ◽  
Vol 44 (4) ◽  
pp. 499-504 ◽  
Author(s):  
M. Van Der Straeten ◽  
A. Vermeulen ◽  
N. Orie ◽  
P. Regniers

ABSTRACT The authors studied the correlation between cortisol production, as measured by an isotope dilution method, and the urinary excretion of total and free Porter-Silber chromogens, as well as of 17-ketogenic steroids. Although a significant correlation exists between total Porter-Silber chromogens, 17-ketogenic steroid excretion and cortisol production, discrepancies are occasionally observed. Hence, different colorimetric methods should be used to assess the glucocorticoid activity of the adrenal cortex.


1962 ◽  
Vol 40 (2) ◽  
pp. 254-262 ◽  
Author(s):  
H. H. Bassøe ◽  
R. Emberland ◽  
E. Glück ◽  
K. F. Støa

ABSTRACT The steroid excretion and the plasma corticosteroids were investigated in three patients with necrosis of the brain and of the pituitary gland. The patients were kept alive by artificial ventilation. In two of the patients the neutral 17-ketosteroids and the 17-hydrocorticosteroids fell to extremely low levels. At the same time, the number of eosinophil cells showed a tendency to increase. Corticotrophin administered intravenously twice to the third patient had a stimulating effect on the adrenal cortex. The theoretical and practical significance of these findings is discussed.


1969 ◽  
Vol 61 (2) ◽  
pp. 219-231 ◽  
Author(s):  
V. H. Asfeldt

ABSTRACT This is an investigation of the practical clinical value of the one mg dexamethasone suppression test of Nugent et al. (1963). The results, evaluated from the decrease in fluorimetrically determined plasma corticosteroids in normal subjects, as well as in cases of exogenous obesity, hirsutism and in Cushing's syndrome, confirm the findings reported in previous studies. Plasma corticosteroid reduction after one mg of dexamethasone in cases of stable diabetes was not significantly different from that observed in control subjects, but in one third of the insulin-treated diabetics only a partial response was observed, indicating a slight hypercorticism in these patients. An insufficient decrease in plasma corticosteroids was observed in certain other conditions (anorexia nervosa, pituitary adenoma, patients receiving contraceptive or anticonvulsive treatment) with no hypercorticism. The physiological significance of these findings is discussed. It is concluded that the test, together with a determination of the basal urinary 17-ketogenic steroid excretion, is suitable as the first diagnostic test in patients in whom Cushing's syndrome is suspected. In cases of insufficient suppression of plasma corticosteroids, further studies, including the suppression test of Liddle (1960), must be carried out.


1947 ◽  
Vol 167 (1) ◽  
pp. 7-25 ◽  
Author(s):  
H. Hirschmann ◽  
Frieda B. Hirschmann

1962 ◽  
Vol 25 (2) ◽  
pp. 199-209 ◽  
Author(s):  
V. WYNN ◽  
J. LANDON ◽  
V. H. T. JAMES

SUMMARY The effect of methandienone administration on urinary steroid excretion has been studied in subjects with normal pituitary-adrenal function and in patients with various endocrine diseases. In the control subjects, a marked suppression of urinary 17-KS and 17-OHCS excretion occurred, which persisted throughout even prolonged periods of methandienone administration. Upon cessation of methandienone treatment a prompt rise in urinary steroid excretion occurred, on occasions to levels slightly higher than those seen before treatment. Similar results were obtained in subjects with acromegaly and Cushing's syndrome, but in patients with anorexia nervosa and a low basal steroid excretion, the suppressive effect of methandienone was less marked. During treatment with methandienone, pituitary response to metopirone was depressed, but adrenal response to corticotrophin was unaltered. It was concluded that methandienone diminishes the rate of production of adrenocortical steroid by inhibiting corticotrophin production or release. Unlike the inhibition observed during treatment with glucocorticoids, it was not associated with atrophy of the adrenal glands.


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