Glucocorticoids have been shown to inhibit GH secretion in normal man when acutely and chronically administered in pharmacological amounts. Pyridostigmine (PD), an acetylcholinesterase inhibitor, is able to elicit GH secretion when administered alone and to enhance the GH response to GHRH in normal subjects probably via a decrease in the hypothalamic release of somatostatin. The aim of the present study was to investigate the influence of glucocorticoids on the GH response to PD administered either alone or in combination with GHRH in normal adult subjects. Six healthy adult volunteers underwent six experimental protocols. They received 1) human (h) GHRH(1-29)NH2, 100 micrograms injected as an iv bolus; 2) cortisone acetate, 50 mg administered orally (po) 60 min before an hGHRH iv bolus injection; 3) PD, 120 mg administered po, 60 min before an hGHRH iv bolus injection; 4) PD and cortisone acetate, administered po 60 min before an hGHRH iv bolus injection; 5) PD, administered po 60 min before a saline iv bolus injection; 6) PD and cortisone acetate administered po 60 min before a saline iv bolus injection. Mean GH levels, peak GH levels, and GH area under the curves (AUCs) were significantly lower after GHRH + cortisone as compared to GHRH alone. However, these parameters were not significantly different after PD + GHRH + cortisone when compared to PD + GHRH and after PD + cortisone when compared to PD alone. We conclude that acute administration of pharmacological amounts of glucocorticoids cannot inhibit the GH response to PD alone or in combination with GHRH. Thus, we hypothesize that the inhibitory action of glucocorticoids on the GH response to GHRH in man may be mediated by an enhancement of either somatostatin release by the hypothalamus or somatostatin action on the pituitary.

Glucocorticoids have been shown to inhibit GH secretion in normal man when administered in large amounts for several days. The aim of our study was 1. to investigate the acute effects of a single dose of glucocorticoids on GH secretion in normal man; 2. to look at the relationship between the increase in serum cortisol concentration and GH response to the stimuli. Six healthy volunteers received on three occasions in random order an iv injection of GHRH (1-29) NH2, 100 \g=m\g, alone or 60 min after oral administration of either 25 or 50 mg of cortisone acetate. Mean stimulated GH levels, GH peak and integrated GH concentration were significantly lower after GHRH plus cortisone 25 mg than after GHRH alone. Mean GH levels at 15 and 30 min after GHRH injection and the peak GH level showed a further decrease after GHRH plus cortisone 50 mg. We conclude that acute administration of pharmacological doses of glucocorticoids is able to inhibit GH response to GHRH, probably through enhancement of endogenous somatostatin release. Moreover, this pharmacological effect of glucocorticoids seems to be dose-dependent and thus directly related to serum cortisol concentrations.Glucocorticoids have long been known to interfere with normal growth, their administration leading to growth retardation in animals (1) as well as in man (2). The role played by glucocorticoids in the regulation of GH secretion is still unclear.Administration of supraphysiological doses of glucocorticoids is able to blunt GH response to var¬ ious pharmacological and physiological stimuli and to diminish GH production rate in normal man (3-7). Moreover, patients with Cushing's disease are known to have reduced GH response to these stim¬ uli, and in some patients with acromegaly GH re¬ sponses to GHRH are decreased by pharmacolog¬ ical doses of glucocorticoids (8-9).On the other hand, several studies have reported that glucocorticoids enhance GH release by cul¬ tured rat and human pituitary somatotropes (10), GH gene transcription (11), and GHRH receptor synthesis (12). In adrenalectomized rats the GH response to GHRH has been clearly shown to depend on the presence of physiological glucocorticoid levels (13). Moreover, GH deficiency in pa¬ tients with idiopathic adrenocorticotropin defi¬ ciency resolves during glucocorticoid replacement (14).Recently, it has been suggested that the contra¬ dictory evidence from in vitro and in vivo studies regarding the effects of glucocorticoids on GH se¬ cretion could be due to in vivo glucocorticoid en¬ hancement of hypothalamic somatostatin release (15).All the cited studies, both those concerning ad¬ ministration of large glucocorticoid doses to normal man and those concerning hypo-or hyperadrenal subjects, did not investigate the relation¬ ship between acute rises in serum cortisol concen¬ trations and pituitary GH responsiveness to the stimuli. Therefore, the aim of our study was 1. to inves¬ tigate the acute effects of a single dose of gluco¬ corticoids on GH secretion in normal man; 2. to look at the relationship be...

Abstract. In vitro studies have demonstrated that thyroid hormones can enhance basal and stimulated growth hormone secretion by cultured pituitary cells. However, both in man and in the rat the effects of high thyroid hormone levels on GH secretion are unclear. The aim of our study was to test the GH response to human GHRH in hyperthyroid patients and to evaluate the effects on GH secretion of short- and long-term pharmacological decrease of circulating thyroid hormones. We examined 10 hyperthyroid patients with recent diagnosis of Graves' disease. Twelve healthy volunteers served as controls. All subjects received a bolus iv injection of GHRH(1-29)NH2, 100 μg. Hyperthyroid patients underwent a GHRH test one and three months after starting antithyroid therapy with methimazole, 10 mg/day po. GH levels at 15, 30, 45, 60 min and GH peak after stimulus were significantly lower in hyperthyroid patients than in normal subjects. The GH peak was also delayed in hyperthyroid patients. After one month of methimazole therapy, most of the hyperthyroid patients had thyroid hormone levels in the normal range, but they did not show significant changes in GH levels after GHRH, and the GH peak was again delayed. After three months of therapy with methimazole, the hyperthyroid patients did not show a further significant decrease in serum thyroid hormone levels. However, mean GH levels from 15 to 60 min were significantly increased compared with the control study. The GH peak after GHRH was also earlier than in the pretreatment study. In conclusion, the GH response to GHRH is inhibited and delayed by hyperthyroidism and returns to the normal pattern after long-term euthyroidism has been achieved with methimazole.

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