Partial Somatotrophin Insufficiency in Cushing's Syndrome

Strauch, G; Modigliani, E; Luton, P; Bricaire, H

doi:10.1530/acta.0.0600121

Cited by 14 publications

(5 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

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 Pituitary ACTH, GH, LH, FSH, TSH and Prolactin Reserves in Patients with Cushing's Syndrome

Hashimoto

1975

Endocrinol Japon

View full text Add to dashboard Cite

In order to know the pituitary reserves of ACTH, GH, LH, FSH, TSH and prolactin in patients with Cushing's syndrome, the responses of these hormones to hydrocortisone, lysine-8 vasopressin (LVP), insulin-induced hypoglycemia, luteinizing hormon-releasing hormone (LH-RH) and thyrotropin releasing hormone (TRH) were examined before and after treatment. Fourteen patients with Cushing's disease (adrenal hyperplasia), 3 patientswith adrenal adenoma and one patient with adrenal carcinoma were investigated. Before treatment, sufficient response of plasma ACTH to LVP was observed in patients with Cushing's disease, while no response was observed in 3 patients with adrenal adenoma. There was no significant difference in the responses of other pituitary hormones between the patients with Cushing's disease. and the patients with adrenal adenoma. The response of plasma GH to insulin-induced hypoglycemia was impaired in most these patients. The response of plasma TSH to TRH was impaired in 6 of 8 patients tested. The response of plasma LH and FSH to LH-RH were preserved in 6 and 5 of 8 patients, respectively. The response of plasma prolactin to TRH was normal in most patients tested. After treatment, the improvements of the impaired responses of GH, TSH, LH and FSH wereobserved. Therefore, the impaired reserve observed in these patients before treatment seemed to be due to the hypercortisolemia. If the difference of the suppressibility of these pituitary hormones by cortisol may be judged simply from our observation, the orderof the suppressibility is supposed to be ACTH, GH, TSH, LH and FSH, and then prolactin.

show abstract

Section: Discussionsupporting

confidence: 92%

The Pituitary ACTH, GH, LH, FSH, TSH and Prolactin Reserves in Patients with Cushing's Syndrome

Hashimoto

1975

Endocrinol Japon

View full text Add to dashboard Cite

show abstract

“…First, GH is certainly not a determining factor. GH response to ornithine stimulation test was normal in 3 cases and depressed in another two (results not shown); similar differences in GH response have been reported by other authors (3)(4)(5)(6)(7)(8)(9)(10). Second, adrenal androgens do not seem to be involved either, since in patients submitted to glucocorticoid therapy (whose adrenals are consequently at rest), serum IGF levels were similar to that found in Cushing's syndrome patients.…”

Section: Discussionsupporting

confidence: 88%

“…There have been conflicting reports concerning the secretion of GH in such cases, both normal and subnormal responses of plasma GH to provocative tests having been observed (3)(4)(5)(6)(7)(8)(9)(10). Simultaneous treatment with glucocorticoids during GH therapy stunts growth if the doses are too high (11) and human GH administration has no effect on the retarded growth of children treated with large doses of glucocorticoid (6,12,13).…”

mentioning

confidence: 99%

Serum Somatomedin/Insulin-Like Growth Factor (IGF) and IGF Carrier Levels in Patients with Cushing's Syndrome or Receiving Glucocorticoid Therapy*

Gourmelen

Girard

Binoux

1982

The Journal of Clinical Endocrinology & Metabolism

View full text Add to dashboard Cite

Serum levels of somatomedin (SM)/insulin-like growth factor (IGF) and IGF carrier (IGF CP) have been determined in 49 patients with Cushing's syndrome before and/or after treatment and in 11 subjects under glucocorticoid therapy.Serum samples were gel filtered in acetic acid in order to separate IGFs from their carriers. IGF content was measured by a competitive protein-binding assay using the specific IGF CP produced by rat liver in culture and human IGF ([ 125 I]IGF I as tracer and a partially purified IGF preparation as standard). IGF CP concentration was assessed in terms of IGF CP binding to labeled IGF, compared to a reference IGF CP preparation obtained from human serum. Results are expressed in comparison with a pool of normal adult serum arbitrarily assigned values of 1 U IGF and 1 U IGF CP per milliliter.The mean IGF level for 39 untreated patients with Cushing's syndrome was 0.99 ± 0.06 (SEM) U/ml, which does not differ from normal adult values (1.05 ± 0.03). Nevertheless, 9 of these patients had subnormal values. For the 14 children or adolescents included in this group, the values observed fell within the range of the controls of the same age, although the growth rate determined for 10 of these patients averaged 1.4 cm/yr.The mean IGF CP level for the untreated patients was 0.78 ± 0.64 U/ml, which is significantly lower than that ol controls.(1.03 ± 0.05; P < 0.001).No correlation was found between IGF or IGF CP levels and parameters reflecting the severity of the hypercortisolism. In the 23 patients investigated after treatment, IGF and IGF CP levels fell within the range of normal values.For the 11 subjects under glucocorticoid therapy the mean IGF and IGF CP levels were no different from control values.Sulfation assays were carried out on the same serum samples as those used for the IGF determinations in 21 of the untreated patients with Cushing's syndrome. The mean SM activity (0.65 ± 0.06 U/ml) was significantly lower than that of controls (0.91 ± 0.04; P < 0.001), which suggests that factors other than IGF are responsible for the depressed SM activity.The conclusion that can be drawn from these findings is that the stunted growth associated with hypercortisolism cannot be attributed to an IGF deficiency. (J Clin Endocrinol Metab 54: 885, 1982) R ETARDED growth associated with either endogenous or exogenous hypercorticism is a well known phenomenon (1, 2) and constitutes one of the signs by which Cushing's syndrome may be diagnosed in young subjects.There have been conflicting reports concerning the secretion of GH in such cases, both normal and subnormal responses of plasma GH to provocative tests having been observed (3-10). Simultaneous treatment with glucocorticoids during GH therapy stunts growth if the doses are too high (11) and human GH administration has no effect on the retarded growth of children treated with large doses of glucocorticoid (6,12,13).A number of studies have demonstrated that glucocorticoids have a direct action on cartilage in addition to inhibiting the stimulatory ...

show abstract

“…Les moyennes sont pr6sent6es avee leurs 6carttypes. [22,28,29,35,37]. c) D'aprgs Miller [22], le diabgte s'am61iore presque toujours et disparMt dans plus de 50% des cas oh le traitement a 6t6 conduit avec succgs, le retour ~ la normale de l'hyperglycgmie ~tant souvent plus long.…”

Section: C) Mdthodesunclassified

“…Cependant, l'existence de faeteurs antagonistes de l'insuline ne peut pas 6tre 6cart6e. Parmi eeux-ci: l'hormone de eroissanee ne pent 6tre retenue comme le montrent les r6sultats de nos dosages radio-immunologiques de STH chez ees m4mes malades [35].…”

Section: Rdsultatsunclassified

Effets du glucose et de l'arginine sur la s�cr�tion d'insuline au cours des syndromes de Cushing

Modigliani¹,

Strauch²,

Luton³

et al. 1970

Diabetologia

Self Cite

View full text Add to dashboard Cite

Partial Somatotrophin Insufficiency in Cushing's Syndrome

Cited by 14 publications

References 0 publications

The Pituitary ACTH, GH, LH, FSH, TSH and Prolactin Reserves in Patients with Cushing's Syndrome

The Pituitary ACTH, GH, LH, FSH, TSH and Prolactin Reserves in Patients with Cushing's Syndrome

Serum Somatomedin/Insulin-Like Growth Factor (IGF) and IGF Carrier Levels in Patients with Cushing's Syndrome or Receiving Glucocorticoid Therapy*

Effets du glucose et de l'arginine sur la s�cr�tion d'insuline au cours des syndromes de Cushing

Contact Info

Product

Resources

About