Corticotropin releasing factor effects on pituitary-adrenal axis before and after ketoconazole in cushing's syndrome

1986 ◽  
Vol 25 ◽  
pp. 142
Author(s):  
M. Boscaro ◽  
A. Rampazzo ◽  
N. Sonino ◽  
F. Mantero
2007 ◽  
Vol 148 (5) ◽  
pp. 195-202 ◽  
Author(s):  
Péter Igaz ◽  
Károly >Rácz ◽  
Miklós Tóth ◽  
Edit Gláz ◽  
Zsolt Tulassay

Iatrogenic Cushing’s syndrome is the most common form of hypercortisolism. Glucocorticoids are widely used for the treatment of various diseases, often in high doses that may lead to the development of severe hypercortisolism. Iatrogenic hypercortisolism is unique, as the application of exogenous glucocorticoids leads to the simultaneous presence of symptoms specific for hypercortisolism and the suppression of the endogenous hypothalamic-pituitary-adrenal axis. The principal question of its therapy is related to the problem of glucocorticoid withdrawal. There is considerable interindividual variability in the suppression and recovery of the hypothalamic-pituitary-adrenal axis, therefore, glucocorticoid withdrawal and substitution can only be conducted in a stepwise manner with careful clinical follow-up and regular laboratory examinations regarding endogenous hypothalamic-pituitary-adrenal axis activity. Three major complications which can be associated with glucocorticoid withdrawal are: i. reactivation of the underlying disease, ii. secondary adrenal insufficiency, iii. steroid withdrawal syndrome. Here, the authors summarize the most important aspects of this area based on their clinical experience and the available literature data.


1987 ◽  
Vol 114 (2) ◽  
pp. 166-170 ◽  
Author(s):  
D. Gordon ◽  
C. G. Semple ◽  
G. H. Beastall ◽  
J. A. Thomson

Abstract. The hypothalamic-pituitary-adrenal axis was investigated in all six patients requiring glucocorticoid replacement 2.5–11 years after unilateral adrenalectomy for adrenal adenomas causing Cushing's syndrome. The hypothalamic-pituitary-adrenal axis was assessed by insulin induced hypoglycaemia and CRF testing in each patient. Two patients showed normal cortisol and ACTH responses to hypoglycaemia. Two patients showed subnormal cortisol responses to hypoglycaemia in the presence of high or normal basal ACTH concentrations. ACTH concentrations increased with both hypoglycaemia and CRF. Two patients showed subnormal cortisol responses to hypoglycaemia and CRF. One of these patients showed an ACTH rise following hypoglycaemia but not CRF. Defects at either hypothalamic-pituitary or adrenal levels were demonstrated and recovery of the axis appears to commence at the hypothalamic-pituitary level.


1974 ◽  
Vol 8 (4) ◽  
pp. 377-377
Author(s):  
Herbert L Vallet ◽  
Edward V Rafuse ◽  
Kathleen A Poon ◽  
Eleanor Grimm ◽  
Lesley S Baldwin ◽  
...  

Author(s):  
K J Malik ◽  
K Wakelin ◽  
S Dean ◽  
D H Cove ◽  
P J Wood

The referral of a patient with features of Cushing's syndrome but with suppressed plasma cortisol and adrenocorticotrophic hormone concentrations prompted us to study the effect of medroxyprogesterone acetate (MPA) therapy on the adrenal axis. 11 women (aged 54–82 years) who were receiving 200–400 mg/day MPA were studied. Of these, four had subnormal plasma cortisol responses to a short synacthen test, and two more had borderline responses (30 min post-synacthen plasma cortisol results of 411 and 511 nmol/L). We conclude that suppression of the adrenal axis occurs relatively frequently in patients on MPA and that such patients should be checked for evidence of suppression before MPA therapy is withdrawn.


1996 ◽  
Vol 21 (7) ◽  
pp. 599-608 ◽  
Author(s):  
Ziad Kronfol ◽  
Monica Starkman ◽  
David E. Schteingart ◽  
Vijendra Singh ◽  
Qun Zhang ◽  
...  

1975 ◽  
Vol 5 (2) ◽  
pp. 165-168 ◽  
Author(s):  
John Johnson

SynopsisA case of Cushing's syndrome in a woman aged 50 years is described, with psychosis of schizophrenic type. The psychosis and endocrine disorder were subsequently cured by adrenalectomy. Twenty-five years previously the patient had a typical schizophrenic psychosis treated in mental hospital with deep insulin therapy and ECT. The possibility is raised that deep insulin therapy could have induced the Cushing's syndrome through its non-specific stressor effect on the pituitary-adrenal axis.


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