1971
DOI: 10.1530/acta.0.0670127
|View full text |Cite
|
Sign up to set email alerts
|

Pituitary Response to Stress in Cushing's Disease

Abstract: Plasma corticosteroids (11-OHCS) and serum immunoreactive growth hormone (IRGH) were measured in six normal subjects during an insulin tolerance test (ITT) and in four patients with normal endocrine function during the first hour of abdominal surgery. Three normal subjects were given a short dexamethasone suppression (1 mg every 6 h for five doses) followed by an ITT 2 h after the last dose. Three patients with normal endocrine function were treated identically, receiving the last dose 2 h before an operation.… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2

Citation Types

1
2
0

Year Published

1973
1973
2017
2017

Publication Types

Select...
5
3

Relationship

1
7

Authors

Journals

citations
Cited by 16 publications
(3 citation statements)
references
References 0 publications
1
2
0
Order By: Relevance
“…The lack of normal growth hormone responsiveness to insulin induced hypoglycemia in our patients is in agreement with that reported in the literature (Frantz et al, 1964;Hartog et al, 1964 , 1968;Strauch et al, 1969;Morrow et al, 1969;Werder et al 1971;Krieger and Glick, 1972;Demura et al, 1972;Werder et al, 1971) reported that the patients with hyper-adrenocorticism showed virtually no growth hormone elevation in response to the stress induced by hypoglycemia, behaving similar to dexamethoasone suppressed subjects. Stiel et al (1970) reported that normal subjects treated for 2 weeks with predonisolone in doses of 15 mg per day showed no significant diminution in their spontaneous plasma GH peaks and postulated that the chronicity, the constancy and the severity of glucocorticoid excess might all be the factors in abolishing the plasma GH peaks in Cushing's syndrome.…”
Section: Discussionsupporting
confidence: 92%
“…The lack of normal growth hormone responsiveness to insulin induced hypoglycemia in our patients is in agreement with that reported in the literature (Frantz et al, 1964;Hartog et al, 1964 , 1968;Strauch et al, 1969;Morrow et al, 1969;Werder et al 1971;Krieger and Glick, 1972;Demura et al, 1972;Werder et al, 1971) reported that the patients with hyper-adrenocorticism showed virtually no growth hormone elevation in response to the stress induced by hypoglycemia, behaving similar to dexamethoasone suppressed subjects. Stiel et al (1970) reported that normal subjects treated for 2 weeks with predonisolone in doses of 15 mg per day showed no significant diminution in their spontaneous plasma GH peaks and postulated that the chronicity, the constancy and the severity of glucocorticoid excess might all be the factors in abolishing the plasma GH peaks in Cushing's syndrome.…”
Section: Discussionsupporting
confidence: 92%
“…The absence of any such changes in subjects with pituitarydependent Cushing's syndrome has also been observed previously. The phenomenon has been attributed by some to an intrinsic hypothalamic defect of the disease (James, Landon, Wynn & Greenwood, 1968), and by others to adrenocortical overactivity (Werder, Smilo, Hane & Forsham, 1971). The latter view is supported by the recent observations of Besser, Cryer & Staub (1972) that such patients do show an in¬ crease of plasma ACTH concentration during insulin-induced hypoglycaemia after adrenalectomy.…”
Section: Discussionmentioning
confidence: 99%
“…This inhibition can be overcome by the stress of surgery, which induces elevated cortisol blood levels despite general anesthesia (9). That halothane anesthesia interferes with steroid biosynthesis directly or enhances catabolism of steroids in the liver is unlikely, since patients with Cushing's syndrome and a fixed steroid output from their adrenal glands show a constant level of plasma 11-OHCS during general anesthesia (10).…”
mentioning
confidence: 99%