Immune regulation in cushing's syndrome: Relationship to hypothalamic-pituitary-adrenal axis hormones

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


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