Neurosurgery restores late GH rise after glucose-induced suppression in cured acromegalics

R. Attanasio, G. Oppizzi, S. Lodrini, D. Dallabonzana, M. Barausse, P. Orlandi, N. DaRe, R. Cozzi

Research output: Contribution to journalArticle

Abstract

Objective and design: A decrease of GH levels below 2 μg/l after an oral glucose tolerance test (OGTT) is still currently accepted as the gold standard for assessing cure in surgically treated acromegaly. Whether glucose-induced suppression of GH is accompanied by a restoration of normal GH late rebound has not yet been evaluated in this disease. In order to assess the restoration of normal GH regulation after removal of a pituitary adenoma, we have evaluated GH changes after an OGTT in a series of selected acromegalic patients (transsphenoidal surgery and lack of pituitary failure). Methods: Twenty-nine patients (13 male, 16 female, age range 27-70 years) entered the study. Their neuroradiological imaging before neurosurgery showed microadenoma in 7, intrasellar macroadenoma in 8 and macroadenoma with extrasellar extension in 14. Plasma GH levels were assayed up to 300 min after glucose administration (75 g p.o.) and IGF-I on basal samples. Results: Basal GH levels were below 5 μg/l in 20 patients and below 2 μg/l in 5 of these. Normal age-adjusted IGF-I levels were observed in 12 patients. GH values were suppressed below 2 μg/1 during an OGTT in 13 patients, and below 1 μg/l in 7 of these. In 9 patients out of these 13, a marked rise in GH levels occurred after nadir. Baseline and nadir GH values of these 9 patients were not different from the corresponding values of the other 4 patients without OGTT-induced late GH peaks. Conclusions: GH rebound after GH nadir occurs in acromegalic patients considered as cured on the basis of OGTT- induced GH suppression and/or IGF-I normalization. The restoration of this physiological response could be regarded as a marker of recovered/preserved integrity of the hypothalamic-pituitary axis. Even though the reason for this GH rebound has not yet been elucidated (GHRH discharge?/end of somatostatin inhibition?), the lack of late GH peak in the patients regarded as cured by the usual criteria could be due to injury to the pituitary stalk caused by the adenoma or by surgical manipulation.

Original languageEnglish
Pages (from-to)23-28
Number of pages6
JournalEuropean Journal of Endocrinology
Volume140
Issue number1
DOIs
Publication statusPublished - Jan 1999

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Neurosurgery
Glucose
Glucose Tolerance Test
Insulin-Like Growth Factor I
Acromegaly
Pituitary Neoplasms
Pituitary Gland
Somatostatin
Adenoma
Wounds and Injuries

ASJC Scopus subject areas

  • Endocrinology

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Attanasio, R., Oppizzi, G., Lodrini, S., Dallabonzana, D., Barausse, M., Orlandi, P., ... Cozzi, R. (1999). Neurosurgery restores late GH rise after glucose-induced suppression in cured acromegalics. European Journal of Endocrinology, 140(1), 23-28. https://doi.org/10.1530/eje.0.1400023

Neurosurgery restores late GH rise after glucose-induced suppression in cured acromegalics. / Attanasio, R.; Oppizzi, G.; Lodrini, S.; Dallabonzana, D.; Barausse, M.; Orlandi, P.; DaRe, N.; Cozzi, R.

In: European Journal of Endocrinology, Vol. 140, No. 1, 01.1999, p. 23-28.

Research output: Contribution to journalArticle

Attanasio, R, Oppizzi, G, Lodrini, S, Dallabonzana, D, Barausse, M, Orlandi, P, DaRe, N & Cozzi, R 1999, 'Neurosurgery restores late GH rise after glucose-induced suppression in cured acromegalics', European Journal of Endocrinology, vol. 140, no. 1, pp. 23-28. https://doi.org/10.1530/eje.0.1400023
Attanasio R, Oppizzi G, Lodrini S, Dallabonzana D, Barausse M, Orlandi P et al. Neurosurgery restores late GH rise after glucose-induced suppression in cured acromegalics. European Journal of Endocrinology. 1999 Jan;140(1):23-28. https://doi.org/10.1530/eje.0.1400023
Attanasio, R. ; Oppizzi, G. ; Lodrini, S. ; Dallabonzana, D. ; Barausse, M. ; Orlandi, P. ; DaRe, N. ; Cozzi, R. / Neurosurgery restores late GH rise after glucose-induced suppression in cured acromegalics. In: European Journal of Endocrinology. 1999 ; Vol. 140, No. 1. pp. 23-28.
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