Recovery of Hypothalamic-Pituitary-Adrenal Function, Growth Hormone Responsiveness and Sleep EEG Pattern in a Patient Following Removal of an Adrenal Cortical Adenoma

1974 ◽  
Vol 38 (6) ◽  
pp. 1075-1082 ◽  
Author(s):  
DOROTHY T. KRIEGER ◽  
GEORGE P. GEWIRTZ
1986 ◽  
Vol 314 (21) ◽  
pp. 1335-1342 ◽  
Author(s):  
Philip W. Gold ◽  
Harry Gwirtsman ◽  
Peter C. Avgerinos ◽  
Lynnette K. Nieman ◽  
William T. Gallucci ◽  
...  

2019 ◽  
Vol 102 ◽  
pp. 128-138 ◽  
Author(s):  
XiaoTing Niu ◽  
XiaoYun Wu ◽  
AnNa Ying ◽  
Bei Shao ◽  
XiaoFeng Li ◽  
...  

1971 ◽  
Vol 50 (1) ◽  
pp. 41-50 ◽  
Author(s):  
HELEN J. STEWART ◽  
E. A. BENSON ◽  
M. MAUREEN ROBERTS ◽  
A. P. M. FORREST ◽  
F. C. GREENWOOD

SUMMARY Plasma growth hormone (GH) levels during insulin hypoglycaemia were measured in 30 women with implants of 90Y in the pituitary for advanced breast cancer. There was evidence of continued pituitary activity in six patients (20%), the rise in plasma GH level being greater than 4 ng/ml during hypoglycaemia. Thirteen patients (43%) were regarded as having complete ablations because they had no GH response and a fasting level of less than 4 ng/ml. In the remaining 11 patients (37%) there was no rise in the GH level during hypoglycaemia, but there were significant fasting levels. From the post-mortem evidence it was concluded that these patients also had adequate ablations. This test is shown to be of more value in estimating residual pituitary function than routine tests of thyroid or adrenal function.


1997 ◽  
Vol 82 (6) ◽  
pp. 1979-1988 ◽  
Author(s):  
John S. Petrides ◽  
Philip W. Gold ◽  
Gregory P. Mueller ◽  
Anita Singh ◽  
Costas Stratakis ◽  
...  

Petrides, John S., Philip W. Gold, Gregory P. Mueller, Anita Singh, Costas Stratakis, George P. Chrousos, and Patricia A. Deuster.Marked differences in functioning of the hypothalamic-pituitary-adrenal axis between groups of men. J. Appl. Physiol. 82(6): 1979–1988, 1997.—To compare profiles of hypothalamic-pituitary-adrenal (HPA) responsiveness, healthy, moderately trained men ( n = 15) were classified as high ( n = 7) or low responders ( n = 8) on the basis of plasma adrenocorticotropic hormone (ACTH) responses to strenuous treadmill exercise 4 h after 4 mg of dexamethasone (Dex). These groups were then evaluated to compare 1) HPA and growth hormone responses to exercise at 90% maximal oxygen uptake 4 h after placebo, Dex (4 mg), and hydrocortisone (100 mg); 2) pituitary-adrenal responses to infusion of arginine vasopressin (AVP); 3) plasma cortisol after a Dex suppression test (1 mg); and 4) behavioral characteristics. In comparison to low responders, high responders exhibited significantly 1) higher plasma ACTH responses to exercise after placebo and Dex; 2) higher plasma AVP secretion with exercise after placebo and marked Dex- and hydrocortisone-induced enhancement of exercise-induced AVP secretion; 3) lower Dex-induced increases in basal and stimulated growth hormone secretion; 4) higher plasma ACTH responses to infusion of AVP; and 5) a trend ( P = 0.09) for higher trait anxiety ratings. Similar suppression of plasma cortisol was noted after 1 mg Dex. We conclude that subgroups of healthy male volunteers exhibit unique profiles of HPA responsiveness. We also believe that glucocorticoid pretreatment combined with strenuous exercise allows functional HPA responsiveness to be distinguished between subgroups of healthy controls and may be useful in the determination of susceptibility to disorders characterized by hyper- and hypo-HPA activation.


2014 ◽  
Vol 16 (3) ◽  
pp. 321-333 ◽  

We review studies with human and nonhuman species that examine the hypothesis that epigenetic mechanisms, particularly those affecting the expression of genes implicated in stress responses, mediate the association between early childhood adversity and later risk of depression. The resulting studies provide evidence consistent with the idea that social adversity, particularly that involving parent-offspring interactions, alters the epigenetic state and expression of a wide range of genes, the products of which regulate hypothalamic-pituitary-adrenal function. We also address the challenges for future studies, including that of the translation of epigenetic studies towards improvements in treatments.


1990 ◽  
Vol 122 (3) ◽  
pp. 385-390 ◽  
Author(s):  
R. C. Castro ◽  
J. G. H. Vieira ◽  
A. R. Chacra ◽  
G. M. Besser ◽  
A. B. Grossman ◽  
...  

Abstract Obese patients are characterised by several neuroendocrine abnormalities, including characteristically a decrease in growth hormone responsiveness to GH-releasing hormone. In normal subjects, the GH response to GHRH is enhanced by the acetylcholinesterase inhibitor, pyridostigmine. We have studied the effect of this drug on GH secretion in gross obesity. Twelve obese patients were studied (mean weight 156% of ideal) and compared with a group of 8 normal volunteers. Each subject was initially studied on two occasions, in random order, with GHRH (1–29) NH2 100 μg iv alone and following pretreatment with pyridostigmine 120 mg orally one hour prior to GHRH. In obese patients, the GH response to GHRH was significantly blunted when compared to controls (GH peak: 20 ± 4 vs 44 ± 16 μg/l; mean ± sem). After pyridostigmine, the response to GHRH was enhanced in the obese subjects, but remained significantly reduced compared to non-obese subjects treated with GHRH and pyridostigmine (GH peak: 30 ± 5 vs 77 ± 20 μg/l, respectively). In 6 subjects, higher doses of GHRH or pyridostigmine did not further increase GH responsiveness in obese patients. Our results suggest that obese patients have a disturbed cholinergic control of GH release, probably resulting from increased somatostatinergic tone. This disturbed regulation may be responsible, at least in part, for the blunted GH responses to provocative stimuli.


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