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肢端肥大症患者中生长激素对下丘脑生长抑素能活性的反应。

Growth hormone response to the hypothalamic somatostatinergic activity in acromegalic patients.

作者信息

Yang I, Park S, Woo J, Kim S, Kim J, Kim Y, Choi Y

机构信息

Department of Internal Medicine, Kyunghee University School of Medicine, Seoul, Korea.

出版信息

J Clin Endocrinol Metab. 1997 Aug;82(8):2492-6. doi: 10.1210/jcem.82.8.4125.

DOI:10.1210/jcem.82.8.4125
PMID:9253323
Abstract

Oral glucose administration suppresses the TRH-induced TSH response by enhancing the hypothalamic somatostatinergic activity (HSA). We assessed the HSA in 13 acromegalic patients by measuring glucose-induced suppression of TRH-stimulated TSH secretion. The HSA showed wide variation with up to 64% suppression. The mean HSA of the patients (25 +/- 6%) did not differ from that in normal young men (19 +/- 4%) in our previous study. Six patients had normal or low HSA, and the other 7 patients had high HSA. The mean TRH-stimulated TSH levels of the patients with normal or low HSA was significantly lower than that of the patients with high HSA (5.13 +/- 0.10 vs. 11.30 +/- 2.80 mU/L). The HSA did not relate to sex, age, tumor size, basal GH levels, the paradoxical responses to TRH and GnRH, octreotide response, or the gsp oncogene. In the combined glucose-TRH test, glucose pretreatment completely suppressed the paradoxical increase in GH level at 30 min in 4 patients. However, it could suppress the paradoxical GH response by only 6-51% in the other 5 patients who also showed the paradoxical response in TRH test. The tumor diameter of patients with good response to the HSA was significantly larger than that of the patients with poor response (31 +/- 5 vs. 14 +/- 2 mm) as was the tumor grade (3.3 +/- 0.3 vs. 1.7 +/- 0.2). This study supports the idea that a reduction of HSA is not a primary cause of acromegaly, and the HSA seems to increase to suppress the autonomous secretion of GH from the pituitary adenomas. HSA as well as the response of tumors to HSA do not determine tumor growth.

摘要

口服葡萄糖通过增强下丘脑生长抑素能活性(HSA)来抑制促甲状腺激素释放激素(TRH)诱导的促甲状腺激素(TSH)反应。我们通过测量葡萄糖诱导的对TRH刺激的TSH分泌的抑制作用,评估了13例肢端肥大症患者的HSA。HSA表现出很大差异,抑制率高达64%。患者的平均HSA(25±6%)与我们之前研究中正常年轻男性的平均HSA(19±4%)没有差异。6例患者的HSA正常或较低,另外7例患者的HSA较高。HSA正常或较低的患者的平均TRH刺激的TSH水平显著低于HSA较高的患者(5.13±0.10 vs. 11.30±2.80 mU/L)。HSA与性别、年龄、肿瘤大小、基础生长激素(GH)水平、对TRH和促性腺激素释放激素(GnRH)的矛盾反应、奥曲肽反应或gsp癌基因无关。在联合葡萄糖-TRH试验中,葡萄糖预处理在4例患者中完全抑制了30分钟时GH水平的矛盾性升高。然而,在另外5例在TRH试验中也表现出矛盾反应的患者中,它只能将矛盾性GH反应抑制6 - 51%。对HSA反应良好的患者的肿瘤直径显著大于反应较差的患者(31±5 vs. 14±2 mm),肿瘤分级也是如此(3.3±0.3 vs. 1.7±0.2)。这项研究支持这样一种观点,即HSA降低不是肢端肥大症的主要原因,并且HSA似乎升高以抑制垂体腺瘤的GH自主分泌。HSA以及肿瘤对HSA的反应并不能决定肿瘤的生长。

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Thyrotropin secretion during oral glucose tolerance test in acromegalic patients and control subjects.
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