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

Citation
R. Attanasio et al., Neurosurgery restores late GH rise after glucose-induced suppression in cured acromegalics, EUR J ENDOC, 140(1), 1999, pp. 23-28
Citations number
18
Categorie Soggetti
Endocrinology, Nutrition & Metabolism
Journal title
EUROPEAN JOURNAL OF ENDOCRINOLOGY
ISSN journal
08044643 → ACNP
Volume
140
Issue
1
Year of publication
1999
Pages
23 - 28
Database
ISI
SICI code
0804-4643(199901)140:1<23:NRLGRA>2.0.ZU;2-9
Abstract
Objective and design: A decrease of GH levels below 2 mu g/l after an oral glucose tolerance test (OGTT) is still currently accepted as the gold stand ard for assessing cure in surgically treated acromegaly. Whether glucose-in duced suppression of GH is accompanied by a restoration of normal GH late r ebound has not yet been evaluated in this disease. In order to assess the r estoration of normal GH regulation after removal of a pituitary adenoma, we have evaluated GH changes after an OGTT in a series of selected acromegali c patients (transsphenoidal surgery and lack of pituitary failure). Methods: Twenty-nine patients (13 male, 16 female, age range 27-70 years) e ntered the study, Their neuroradiological imaging before neurosurgery showe d microadenoma in 7, intrasellar macroadenoma in 8 and macroadenoma with ex trasellar extension in 14. Plasma GH levels were assayed up to 300 min afte r glucose administration (75 g p.o.) and IGF-I on basal samples, Results: Basal GH levels were below 5 mu g/l in 20 patients and below 2 mu g/l in 5 of these, Normal age-adjusted IGF-I levels were observed in 12 pat ients. GH values were suppressed below 2 mu g/l during an OGTT in 13 patien ts, and below 1 mu g/l in 7 of these. In 9 patients out of these 13, a mark ed 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 ot her 1. patients without OGTT-induced late GH peaks. Conclusions: GH rebound after GH nadir occurs in acromegalic patients consi dered as cured on the basis of OGTT-induced GH suppression and/or IGF-I nor malization, The restoration of this physiological response could be regarde d as a marker of recovered/preserved integrity of the hypothalamic-pituitar y axis. Even though the reason for this GH rebound has not yet been elucida ted (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 t o injury to the pituitary stalk caused by the adenoma or by surgical manipu lation.