scholarly journals Endocrine Diseases of Ferrets

Author(s):  
Nico J. Schoemaker ◽  
Yvonne R.A. van Zeeland
Keyword(s):  
1974 ◽  
Vol 76 (4) ◽  
pp. 729-740 ◽  
Author(s):  
Peter Kamp ◽  
Per Platz ◽  
Jørn Nerup

ABSTRACT By means of an indirect immunofluorescence technique, sera from 116 patients with Addison's disease, an equal number of age and sex matched controls and 97 patients with other endocrine diseases were examined for the occurrence of antibody to steroid-producing cells in ovary, testis and adrenal cortex. Fluorescent staining was observed in the theca cells of growing follicles, the theca lutein cells, testicular Leydig cells and adrenal cortical cells, i. e. cells which contain enzyme systems used in steroid hormone production. The "steroid-cell" antibody was present in 24 % of the patients with idiopathic Addison's disease, equally frequent in males and females, and in 17 % of the patients with tuberculous Addison's disease, but was rarely found in controls, including patients with other endocrine diseases. Female hypergonadotrophic hypogonadism made an exception, since the "steroid-cell" antibody was found in about half the cases with this condition.


2019 ◽  
Vol 17 (4) ◽  
pp. 118-122
Author(s):  
I. V. Madyanov ◽  
◽  
T. S. Madyanovа ◽  

2019 ◽  
Vol 3 (3) ◽  
pp. 181-189 ◽  
Author(s):  
Jonathan T Avila ◽  
KT Park ◽  
Neville H Golden

2020 ◽  
Vol 11 ◽  
Author(s):  
Louise Magnusson ◽  
Daniel Espes ◽  
Rosaura Casas ◽  
Per-Ola Carlsson

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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