Acute effects of a single administration of dexamethasone on basal and growth hormone-releasing hormone stimulated GH secretion in acromegaly

M. Losa, M. Arosio, A. Cusin, O. Biella, E. Palmieri, G. Faglia, M. Giovanelli

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

A single administration of dexamethasone causes both an early stimulatory and a late inhibitory effect on GH secretion in normal subjects. Objective - We investigated the effects of a single administration of dexamethasone on basal and GH-releasing hormone-stimulated GH secretion in eight patients with active acromegaly. Design - On three different days the patients received 4 mg i.v. dexamethasone, 1 μg/kg body weight GH-releasing hormone 1-29, or matched placebos in different order. Patients - Eight subjects with active acromegaly, five of whom had not been treated previously, while the other three had received octreotide therapy which was stopped at least 7 days before testing. Measurements - Serum GH levels were measured in duplicate by a commercially available RIA kit. Results - Dexamethasone administration caused a significant decline of mean ± SE GH levels from 51.8 ± 13.8 to 30.0 ± 9.2 mU/I at 180 minutes, that was not influenced by placebo administration at 180 minutes. On the contrary, when GH-releasing hormone substituted placebo administration, GH levels increased from 34.0 ± 9.8 mU/I at 180 minutes to 56.0 ± 15.6 mU/I at 195 minutes. The GH increase was higher when GH-releasing hormone was given without dexamethasone pretreatment (from 52.4 ± 13.0 mU/I at 180 minutes to 86.4 ± 25.4 mU/I at l95 minutes). Analysis of the GH area under the curve confirmed the significant inhibition of GH secretion after dexamethasone administration and the significant reduction of the GH response to GH releasing hormone in the study with dexamethasone pretreatment. Conclusions - At variance with data in normal subjects, acute i.v. administration of dexamethasone inhibits basal GH secretion and partially suppresses the GH response to GH-releasing hormone in acromegaly. Both alterations in the regulatory mechanism of adenomatous cells and perturbations of hypothalamic regulatory influences, induced by the state of chronic GH hypersecretion, are likely explanations of the different response to dexamethasone.

Original languageEnglish
Pages (from-to)187-191
Number of pages5
JournalClinical Endocrinology
Volume40
Issue number2
Publication statusPublished - 1994

Fingerprint

Growth Hormone-Releasing Hormone
Acromegaly
Dexamethasone
Hormones
Placebos
Octreotide
Area Under Curve
Body Weight

ASJC Scopus subject areas

  • Endocrinology

Cite this

Acute effects of a single administration of dexamethasone on basal and growth hormone-releasing hormone stimulated GH secretion in acromegaly. / Losa, M.; Arosio, M.; Cusin, A.; Biella, O.; Palmieri, E.; Faglia, G.; Giovanelli, M.

In: Clinical Endocrinology, Vol. 40, No. 2, 1994, p. 187-191.

Research output: Contribution to journalArticle

@article{ccb30b807a53410db40c50171b0de804,
title = "Acute effects of a single administration of dexamethasone on basal and growth hormone-releasing hormone stimulated GH secretion in acromegaly",
abstract = "A single administration of dexamethasone causes both an early stimulatory and a late inhibitory effect on GH secretion in normal subjects. Objective - We investigated the effects of a single administration of dexamethasone on basal and GH-releasing hormone-stimulated GH secretion in eight patients with active acromegaly. Design - On three different days the patients received 4 mg i.v. dexamethasone, 1 μg/kg body weight GH-releasing hormone 1-29, or matched placebos in different order. Patients - Eight subjects with active acromegaly, five of whom had not been treated previously, while the other three had received octreotide therapy which was stopped at least 7 days before testing. Measurements - Serum GH levels were measured in duplicate by a commercially available RIA kit. Results - Dexamethasone administration caused a significant decline of mean ± SE GH levels from 51.8 ± 13.8 to 30.0 ± 9.2 mU/I at 180 minutes, that was not influenced by placebo administration at 180 minutes. On the contrary, when GH-releasing hormone substituted placebo administration, GH levels increased from 34.0 ± 9.8 mU/I at 180 minutes to 56.0 ± 15.6 mU/I at 195 minutes. The GH increase was higher when GH-releasing hormone was given without dexamethasone pretreatment (from 52.4 ± 13.0 mU/I at 180 minutes to 86.4 ± 25.4 mU/I at l95 minutes). Analysis of the GH area under the curve confirmed the significant inhibition of GH secretion after dexamethasone administration and the significant reduction of the GH response to GH releasing hormone in the study with dexamethasone pretreatment. Conclusions - At variance with data in normal subjects, acute i.v. administration of dexamethasone inhibits basal GH secretion and partially suppresses the GH response to GH-releasing hormone in acromegaly. Both alterations in the regulatory mechanism of adenomatous cells and perturbations of hypothalamic regulatory influences, induced by the state of chronic GH hypersecretion, are likely explanations of the different response to dexamethasone.",
author = "M. Losa and M. Arosio and A. Cusin and O. Biella and E. Palmieri and G. Faglia and M. Giovanelli",
year = "1994",
language = "English",
volume = "40",
pages = "187--191",
journal = "Clinical Endocrinology",
issn = "0300-0664",
publisher = "Wiley-Blackwell",
number = "2",

}

TY - JOUR

T1 - Acute effects of a single administration of dexamethasone on basal and growth hormone-releasing hormone stimulated GH secretion in acromegaly

AU - Losa, M.

AU - Arosio, M.

AU - Cusin, A.

AU - Biella, O.

AU - Palmieri, E.

AU - Faglia, G.

AU - Giovanelli, M.

PY - 1994

Y1 - 1994

N2 - A single administration of dexamethasone causes both an early stimulatory and a late inhibitory effect on GH secretion in normal subjects. Objective - We investigated the effects of a single administration of dexamethasone on basal and GH-releasing hormone-stimulated GH secretion in eight patients with active acromegaly. Design - On three different days the patients received 4 mg i.v. dexamethasone, 1 μg/kg body weight GH-releasing hormone 1-29, or matched placebos in different order. Patients - Eight subjects with active acromegaly, five of whom had not been treated previously, while the other three had received octreotide therapy which was stopped at least 7 days before testing. Measurements - Serum GH levels were measured in duplicate by a commercially available RIA kit. Results - Dexamethasone administration caused a significant decline of mean ± SE GH levels from 51.8 ± 13.8 to 30.0 ± 9.2 mU/I at 180 minutes, that was not influenced by placebo administration at 180 minutes. On the contrary, when GH-releasing hormone substituted placebo administration, GH levels increased from 34.0 ± 9.8 mU/I at 180 minutes to 56.0 ± 15.6 mU/I at 195 minutes. The GH increase was higher when GH-releasing hormone was given without dexamethasone pretreatment (from 52.4 ± 13.0 mU/I at 180 minutes to 86.4 ± 25.4 mU/I at l95 minutes). Analysis of the GH area under the curve confirmed the significant inhibition of GH secretion after dexamethasone administration and the significant reduction of the GH response to GH releasing hormone in the study with dexamethasone pretreatment. Conclusions - At variance with data in normal subjects, acute i.v. administration of dexamethasone inhibits basal GH secretion and partially suppresses the GH response to GH-releasing hormone in acromegaly. Both alterations in the regulatory mechanism of adenomatous cells and perturbations of hypothalamic regulatory influences, induced by the state of chronic GH hypersecretion, are likely explanations of the different response to dexamethasone.

AB - A single administration of dexamethasone causes both an early stimulatory and a late inhibitory effect on GH secretion in normal subjects. Objective - We investigated the effects of a single administration of dexamethasone on basal and GH-releasing hormone-stimulated GH secretion in eight patients with active acromegaly. Design - On three different days the patients received 4 mg i.v. dexamethasone, 1 μg/kg body weight GH-releasing hormone 1-29, or matched placebos in different order. Patients - Eight subjects with active acromegaly, five of whom had not been treated previously, while the other three had received octreotide therapy which was stopped at least 7 days before testing. Measurements - Serum GH levels were measured in duplicate by a commercially available RIA kit. Results - Dexamethasone administration caused a significant decline of mean ± SE GH levels from 51.8 ± 13.8 to 30.0 ± 9.2 mU/I at 180 minutes, that was not influenced by placebo administration at 180 minutes. On the contrary, when GH-releasing hormone substituted placebo administration, GH levels increased from 34.0 ± 9.8 mU/I at 180 minutes to 56.0 ± 15.6 mU/I at 195 minutes. The GH increase was higher when GH-releasing hormone was given without dexamethasone pretreatment (from 52.4 ± 13.0 mU/I at 180 minutes to 86.4 ± 25.4 mU/I at l95 minutes). Analysis of the GH area under the curve confirmed the significant inhibition of GH secretion after dexamethasone administration and the significant reduction of the GH response to GH releasing hormone in the study with dexamethasone pretreatment. Conclusions - At variance with data in normal subjects, acute i.v. administration of dexamethasone inhibits basal GH secretion and partially suppresses the GH response to GH-releasing hormone in acromegaly. Both alterations in the regulatory mechanism of adenomatous cells and perturbations of hypothalamic regulatory influences, induced by the state of chronic GH hypersecretion, are likely explanations of the different response to dexamethasone.

UR - http://www.scopus.com/inward/record.url?scp=0028337257&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028337257&partnerID=8YFLogxK

M3 - Article

VL - 40

SP - 187

EP - 191

JO - Clinical Endocrinology

JF - Clinical Endocrinology

SN - 0300-0664

IS - 2

ER -