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The effect of short‐term cortisol changes on growth hormone responses to the pyridostigmine‐growth‐hormone‐releasing‐hormone test in healthy adults and patients with suspected growth hormone deficiency
Author(s) -
Andersen Marianne,
Støving Rene K.,
Hangaard Jørgen,
Petersen Per H.,
Hagen Claus
Publication year - 1998
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1046/j.1365-2265.1998.00529.x
Subject(s) - medicine , endocrinology , pyridostigmine , growth hormone–releasing hormone , hormone , glucocorticoid , hydrocortisone , placebo , growth hormone deficiency , adrenocorticotropic hormone , growth hormone , myasthenia gravis , alternative medicine , pathology
BACKGROUND AND AIMS The interaction between cortisol and growth hormone (GH)‐levels may significantly influence GH‐responses to a stimulation test. In order to systematically analyse the interaction in a paired design, it is necessary to use a test, which has been proven safe and reliable such as the pyridostigmine‐growth‐hormone‐releasing‐hormone (PD‐GHRH) test. Three groups of subjects with a different GH‐secretory capacity were included. STUDY A Eight healthy adults were tested seven times, once with placebo throughout the examination and six times with the PD‐GHRH test following no glucocorticoid pretreatment, pretreatment with hydrocortisone (HC) (30 mg/day and 80 mg/day for 1 and 3 days) or pretreatment with 15 mg prednisolone for 1 day. HC (80 mg/day for 1 day) in combination with PD significantly stimulated GH‐levels compared to PD alone, 18.9 mU/l ± 6.1 vs 3.0 mU/l ± 0.8 ( P < 0.05). However, peak GH‐responses to PD in combination with GHRH were reduced during HC (80 mg/day for 1 day) compared to no glucocorticoid pretreatment in all healthy adults. Conventional HC therapy (30 mg/day for 1 and 3 days) did not significantly affect peak GH‐responses. STUDY B 16 patients with suspected GH‐deficiency (GHD) (seven with known ACTH‐deficiency and nine with an intact pituitary‐adrenal axis) were tested five times with the PD‐GHRH test following no pretreatment or pretreatment with HC (30 mg/day and 80 mg/day for 1 and 3 days). Peak GH‐responses were not significantly affected by conventional HC therapy (30 mg/day for 1 and 3 days). However, peak GH‐responses to PD in combination with GHRH were reduced during HC (80 mg/day for 1 day) compared to no glucocorticoid pretreatment in all patients. Short‐term hypocortisolism did not significantly affect peak GH‐responses. CONCLUSION The GH‐responses to a PD‐GHRH test were reduced in all individuals during acute stress‐appropriate cortisol levels and the percentage reduction in GH‐levels was independent of the GH‐secretory capacity. Clinically, we found that peak GH‐responses were not significantly affected by a short break in conventional HC therapy nor by conventional HC therapy itself. However, our results also demonstrated that a GH‐stimulation test should not be performed on patients, suffering from acute stress.