Corticoid-induced growth hormone (GH) secretion in GH-deficient and normal children.

Martul, P.; Pineda, J; Diéguez, Carlos; Casanueva, Felipe F.

doi:10.1210/jcem.75.2.1639956

Cited by 12 publications

(16 citation statements)

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“…Examples are aminophylline and amphetamines. High cortisol [17, 69]and low thyroid hormone levels decrease peak responses to pharmacological stimuli. Any medication that causes hypoglycemia will increase the response.…”

Section: Sources Of Variation Of Gh Provocative Test Resultsmentioning

confidence: 99%

Interpretative Difficulties with Growth Hormone Provocative Retesting in Childhood-Onset Growth Hormone Deficiency

et al. 1999

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A review of literature demonstrates that there are many ill-understood factors that determine the results of GH provocative (re)testing, so that these results should be interpreted with extreme caution when used for diagnosis or confirmation of diagnosis of GHD. GH provocation tests are probably of no value at all for what has been called ‘partial GHD’. The phenomenon of ‘normalization’ of test results after long-term treatment with GH needs no ‘transient GHD’ hypothesis as it can be largely explained by the very low reproducibility of the tests and by a regression to the mean effect. Moreover, it is possible that ‘normal values’ increase with age. Other determinants of normal peak values may also change from childhood to adulthood and contribute to ‘normalization’.

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Section: Sources Of Variation Of Gh Provocative Test Resultsmentioning

confidence: 99%

Interpretative Difficulties with Growth Hormone Provocative Retesting in Childhood-Onset Growth Hormone Deficiency

et al. 1999

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“…It has been hypothesized that the locus of action of glu cocorticoids to stimulate GH release is the hypothalamic area [10]; the precise mechanism and locus of action of such steroid compounds, however, is still debated. In the present work, dexamethasone was employed as GH stim ulant in both normal subjects and patients affected with different types of hypothalamic or pituitary tumors.…”

Section: Introductionmentioning

confidence: 99%

Modulation by Glucocorticoids of Growth Hormone Secretion in Patients with Different Pituitary Tumors

Popović¹,

Damjanović²,

Micić³

et al. 1993

Neuroendocrinology

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The acute administration of glucocorticoids is a new stimulus of growth hormone (GH) secretion in man. In order to ascertain its point of action, and also the suitability of this new test as a diagnostic tool in GH pathological states, 33 subjects were studied. Eight of them were normal controls, and 25 were patients with tumors affecting the hypothalamopituitary area. A glucocorticoid stimulus, dexamethasone 4 mg i.v. was administered at 0 min and GH levels (means ± SEM, µg/l) were measured during the following 5 h. In addition, GH-releasing hormone (GHRH) and clonidine were employed as either pituitary or hypothalamic GH stimuli. Dexamethasone administration to normal subjects did not alter GH levels in the first 2 h of the test. Afterwards, a GH peak was observed around the third hour, GH levels returning to basal ones thereafter. The dexamethasone-induced GH peak (6.7 ± 1.5) and area under the curve (526 ± 137) were lower than after GHRH (14.0 ± 4.5 and 1,070 ± 369, respectively). In the 14 acromegalic patients studied, the GHRH-induced GH net increase was similar to that observed in controls, while the placebo did not alter GH basal levels. An absence of hypothalamic control was evident because clonidine did not stimulate GH release. On the other hand, and contrary to normal subjects, dexamethasone strongly inhibited GH secretion, the values being significantly lower when calculated either as mean GH peak, or maximum GH increment (Δ). The Δ GH was -2.5 ± 3.1 after placebo, +3.7 ± 4.5 after clonidine, +17.0 ± 3.3 after GHRH and -13.4 ± 4.5 following dexamethasone administration. In 4 patients harboring pituitary prolactinomas, dexamethasone stimulated GH secretion in 1 subject with a microadenoma but was devoid of action in the 3 marcoprolactinoma patients, which had suprasellar extension and absent clonidine-induced GH secretion. Similarly, in 4 out of 5 patients with nonsecreting pituitary adenomas that had a functional pituitary stalk section (suprasellar extension, mild prolactin levels and no GH response to hypothalamic stimulus), dexamethasone was ineffective, while it stimulated GH secretion in the other patient of this group with a normal hypothalamopituitary connection. In addition, in 2 other patients with hypothalamic germinoma and well-preserved GH response to GHRH, dexamethasone was devoid of action. These results indicate that GH stimulation by glucocorticoid is only observed in normal subjects and requires a normal hypothalamopituitary connection. On the contrary, in acromegaly, glucocorticoids induced, instead, an inhibition of GH secretion. In conclusion, glucocorticoid stimulatory action over GH secretion seems to be exerted at the hypothalamic level. On the contrary, in acromegalic patients a ‘paradoxical’ inhibition of GH secretion is observed after glucocorticoid injection. Acute administration of glucocorticoids may be a suitable test in the diagnosis and follow-up of GH pathological states.

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“…In humans administration of glucocorticoid has been shown to increase endogenous GH secretion [12, 14, 16, 26]whereas the effect of glucocorticoid administration on GH release during GH stimulation test are ambiguous as both blunted and enhanced responses have been reported [5, 6, 7]. During glucocorticoid exposure increased levels of IGF-I has frequently been described [1, 2, 5, 8, 11, 12, 13, 14, 15, 16], although some studies found no changes [9, 10, 17, 18].…”

Section: Discussionmentioning

confidence: 99%

No Influence of Prednisolone on IGFBP-3 Proteolysis in Healthy Young Men

et al. 2001

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Aims: The impact of growth hormone (GH) and prednisolone on the GH/insulin-like growth factor (IGF) axis with special emphasis on IGF binding protein-3 (IGFBP-3) proteolysis was studied in 8 healthy adults in a double-blind cross-over study with four periods: (1) placebo; (2) s.c. GH 0.1 IU/kg/day; (3) oral prednisolone 50 mg/day, and (4) co-administration of GH and prednisolone. Methods: Each treatment period lasted for 4 days followed by a washout period of 10 days. We measured IGF-I, IGF-II, IGFBP-1, IGFBP-2, IGFBP-3 by immunoassays, IGFBP-3 by Western ligand blotting (WLB) and finally in vitro IGFBP-3 proteolysis by a ¹²⁵I-IGFBP-3 degradation assay. Results: IGF-I levels increased by 99% during GH administration and 67% during co-administration of GH and prednisolone (p < 0.0005), whereas no significant change was seen during prednisolone alone. IGFBP-1 levels decreased 55% during the prednisolone period (p < 0.002), but the between period changes were not significant (p < 0.1). IGFBP-2 decreased 33% during co-administration of GH and prednisolone (p < 0.002). IGFBP-3 increased 12% during GH and 7% during co-administration of GH and prednisolone (p < 0.003 and p < 0.03 compared to placebo, respectively), whereas prednisolone alone induced no significant changes. IGFBP-3 measured by WLB did not change significantly, neither did IGFBP-3 proteolysis. Conclusions: Prednisolone administration induces only minimal changes in circulating components of the IGF axis and is not accompanied by alterations in IGFBP-3 proteolysis. This indicates that the metabolic effects of glucocorticoids do not depend on serum IGF-I.

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Corticoid-induced growth hormone (GH) secretion in GH-deficient and normal children.

Cited by 12 publications

References 0 publications

Interpretative Difficulties with Growth Hormone Provocative Retesting in Childhood-Onset Growth Hormone Deficiency

Interpretative Difficulties with Growth Hormone Provocative Retesting in Childhood-Onset Growth Hormone Deficiency

Modulation by Glucocorticoids of Growth Hormone Secretion in Patients with Different Pituitary Tumors

No Influence of Prednisolone on IGFBP-3 Proteolysis in Healthy Young Men

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