This Article Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by MIELL, J. P. Articles by GAILLARD, R. C. Search for Related Content PubMed PubMed Citation Articles by MIELL, J. P. Articles by GAILLARD, R. C.

Effects of Dexamethasone on Growth Hormone (GH)-Releasing Hormone, Arginine- and Dopaminergic Stimulated GH Secretion, and Total Plasma Insulin-Like Growth Factor-I Concentrations in Normal Male Volunteers^*

JOHN P. MIELL, ROGER CORDER, FRANÇOIS P. PRALONG and ROLF C. GAILLARD

Neuroendocrine Unit, Department of Medicine, University Hospital of Geneva 1211 Geneva 4, Switzerland

In man, glucocorticoid treatment and endogenous corticosteroid excess generally suppress stimulated GH release. However, such effects are not entirely consistent and depend on both the duration of pituitary exposure to steroids and the secretagogue employed. To further evaluate the effects of glucocorticoids in man, we have studied the response to four different GH stimulation tests before and after treatment with dexamethasone (DEX; 2 mg twice daily during 84 h). Twelve healthy male volunteers were divided into two groups of six subjects (groups A and B). Group A underwent stimulation tests with arginine (500 mg/kg, iv) and GH-releasing hormone (GHRH, 100 µg, iv) before and after DEX treatment. Group B were subjected to stimulation tests with two dopaminergic agents, a novel nonergot D₂-dopamine agonist CV205–502 (CV; 10 µg, iv) and dopamine (4 µg/kg·min, iv), before and after DEX. Within each group, the effect of DEX on the different secretagogues was studied 4 weeks apart. GHRH-stimulated GH release was significantly blunted by DEX treatment [median peak GH value, 34.2 µg/L; 25–75th percentiles, 22.1–56.2), control, vs. 19.8 (9.7–34.5), DEX; P < 0.05; integrated GH secretion expressed as the area under the curve (AUC) was 48% lower after DEX; P < 0.01]. In the same group, DEX treatment significantly enhanced the response to arginine [10.6 (8.0–22.8), control, vs. 26.1 (15.1–38.6), DEX; P < 0.01; with an increase in AUC of 72%; P < 0.01]. In group B, under control conditions before glucocorticoid administration, the GH response to CV was significantly greater than that to dopamine in terms of both peak response [25.1 (8.6–30.9), CV, vs. 11.8 (5.5–16.4), dopamine; P < 0.05] and AUC [2406 ± 654 (CV) vs. 658 ± 125 (dopamine); P < 0.01], suggesting that CV may be a useful adjunct in the diagnosis of GH deficiency. After DEX administration, responses to both dopaminergic agents were suppressed [CV, 6.7 (4.0–21.2); P < 0.01 vs. control response; and dopamine, 5.3 (4.8–7.9); P < 0.05 vs. control response]. When compared with the effects of dexamethasone on the GH response to arginine, the results with dopaminergic agents highlight important differences in the mechanisms of action of these indirectly acting GH secretagogues. Moreover, this may be of physiological importance, because in contrast to the inhibitory effect of glucocorticoid on GHRH-stimulated GH release, DEX treatment significantly increased basal plasma GH levels [1.4 (0.5–5.1) vs. control 0.3 (0.1–0.6) µg/L; P < 0.001]. In addition, basal (0830 h) total plasma IGF-I levels measured after acid-ethanol extraction were significantly increased after DEX (417.0 ± 15.6; control, 300.1 ± 14.4 Mg/L; P < 0.001).

^* This work was supported by Swiss National Research Foundation Grant 3.091.087.

Present address: Programmed Investigation Unit, Department of Medicine, King’s College Hospital, Denmark Hill, London, SE5 8RX United Kingdom.

To whom all correspondence and requests for reprints should be addressed.

Received August 9, 1990.

This article has been cited by other articles:

				E. Charmandari, S. M. Pincus, D. R. Matthews, A. Johnston, C. G. D. Brook, and P. C. Hindmarsh Oral Hydrocortisone Administration in Children with Classic 21-Hydroxylase Deficiency Leads to More Synchronous Joint GH and Cortisol Secretion J. Clin. Endocrinol. Metab., May 1, 2002; 87(5): 2238 - 2244. [Abstract] [Full Text] [PDF]

				S. Bechtold, P. Ripperger, D. Muhlbayer, H. Truckenbrodt, R. Hafner, O. Butenandt, and H. P. Schwarz GH Therapy in Juvenile Chronic Arthritis: Results of a Two-Year Controlled Study on Growth and Bone J. Clin. Endocrinol. Metab., December 1, 2001; 86(12): 5737 - 5744. [Abstract] [Full Text] [PDF]

				E. Charmandari, S. M. Pincus, D. R. Matthews, E. Dennison, C. H. D. Fall, and P. C. Hindmarsh Joint Growth Hormone and Cortisol Spontaneous Secretion Is More Asynchronous in Older Females Than in Their Male Counterparts J. Clin. Endocrinol. Metab., July 1, 2001; 86(7): 3393 - 3399. [Abstract] [Full Text] [PDF]

				A. J. Cleare, S. S. Sookdeo, J. Jones, V. O’Keane, and J. P. Miell Integrity of the Growth Hormone/Insulin-Like Growth Factor System Is Maintained in Patients with Chronic Fatigue Syndrome J. Clin. Endocrinol. Metab., April 1, 2000; 85(4): 1433 - 1439. [Abstract] [Full Text]

				R. K. Støving, J. D. Veldhuis, A. Flyvbjerg, J. Vinten, J. Hangaard, O. G. Koldkjær, J. Kristiansen, and C. Hagen Jointly Amplified Basal and Pulsatile Growth Hormone (GH) Secretion and Increased Process Irregularity in Women with Anorexia Nervosa: Indirect Evidence for Disruption of Feedback Regulation within the GH-Insulin-Like Growth Factor I Axis J. Clin. Endocrinol. Metab., June 1, 1999; 84(6): 2056 - 2063. [Abstract] [Full Text]

				D. B. Allen, J. R. Julius, T. J. Breen, and K. M. Attie Treatment of Glucocorticoid-Induced Growth Suppression with Growth Hormone J. Clin. Endocrinol. Metab., August 1, 1998; 83(8): 2824 - 2829. [Abstract] [Full Text]