Attanasio R, Oppizzi G, Lodrini S, Dallabonzana D, Barausse M, Orlandi P, DaRe N, Cozzi R
Department of Endocrinology, Niguarda Hospital, Milan, Italy.
Eur J Endocrinol. 1999 Jan;140(1):23-8. doi: 10.1530/eje.0.1400023.
A decrease of GH levels below 2 microg/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).
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.
Basal GH levels were below 5 microg/l in 20 patients and below 2 microg/l in 5 of these. Normal age-adjusted IGF-I levels were observed in 12 patients. GH values were suppressed below 2 microg/l during an OGTT in 13 patients, and below 1 microg/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.
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.
口服葡萄糖耐量试验（OGTT）后生长激素（GH）水平降至2μg/L以下目前仍被视为评估手术治疗肢端肥大症治愈情况的金标准。在该疾病中，葡萄糖诱导的GH抑制是否伴随着正常GH晚期反跳的恢复尚未得到评估。为了评估垂体腺瘤切除后正常GH调节的恢复情况，我们在一系列选定的肢端肥大症患者（经蝶窦手术且无垂体功能减退）中评估了OGTT后的GH变化。
29例患者（13例男性，16例女性，年龄范围27 - 70岁）进入研究。他们神经外科手术前的神经影像学检查显示，7例为微腺瘤，8例为鞍内大腺瘤，14例为鞍外扩展的大腺瘤。在口服葡萄糖（75g）后300分钟内测定血浆GH水平，并在基础样本中测定胰岛素样生长因子-I（IGF-I）。
20例患者的基础GH水平低于5μg/L，其中5例低于2μg/L。12例患者观察到年龄调整后的IGF-I水平正常。13例患者在OGTT期间GH值被抑制至低于2μg/L，其中7例低于1μg/L。在这13例患者中的9例，GH水平在最低点后出现显著升高。这9例患者的基线和最低点GH值与其他4例无OGTT诱导的晚期GH峰值的患者的相应值无差异。
在基于OGTT诱导的GH抑制和/或IGF-I正常化被视为治愈的肢端肥大症患者中，GH最低点后会出现GH反跳。这种生理反应的恢复可被视为下丘脑 - 垂体轴完整性恢复/保留的标志。尽管这种GH反跳的原因尚未阐明（促生长激素释放激素释放？/生长抑素抑制结束？），但按照通常标准被视为治愈的患者缺乏晚期GH峰值可能是由于腺瘤或手术操作导致垂体柄损伤。
