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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 M, Stoving RK, Hangaard J, Petersen PH, Hagen C

Affiliation(s): Department of Endocrinology, Odense University Hospital, Denmark. mar.andersen@winsloew.ou.dk

Publication date & source: 1998-08, Clin Endocrinol (Oxf)., 49(2):241-9.

Publication type: Clinical Trial; Randomized Controlled Trial

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.

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