Salerno F, Cocchi D, Lampertico M, Manneschi M, Monza G, Müller E E
Horm Metab Res. 1982 Sep;14(9):482-6. doi: 10.1055/s-2007-1019053.
Patients with chronic liver diseases were evaluated for: 1) the ability of somatostatin to affect the thyrotropin-releasing hormone (TRH) induced growth hormone (GH) rise; 2) the competence of luteinizing-hormone releasing hormone (LH-RH) to release GH; 3) the non-specific releasing effect of TRH and LH-RH on other anterior pituitary (AP) hormones. In 6 patients, infusion of somatostatin (100 micrograms iv bolus + 375 micrograms i.v. infusion) completely abolished the TRH (400 micrograms i.v.)-induced GH rise; in none of 12 patients, of whom 7 were GH-responders to TRH, did LH-RH (100 micrograms i.v.) cause release of GH; 4) finally, LH-RH (12 patients) did not increase plasma prolactin (PRL) and TRH (7 patients) did not evoke a non-specific release of gonadotropins. It is concluded that: 1) abnormal GH-responsiveness to TRH is the unique alteration in AP responsiveness to hypothalamic hormones present in liver cirrhosis; 2) the mechanism(s) subserving the altered GH response to TRH is different from that underlying the TRH-induced GH rise present in another pathologic state i.e. acromegaly, a condition in which the effect of TRH escapes somatostatin suppression and LH-RH evokes GH and PRL release.
1）生长抑素影响促甲状腺激素释放激素（TRH）诱导的生长激素（GH）升高的能力；2）促黄体生成素释放激素（LH-RH）释放GH的能力；3）TRH和LH-RH对其他垂体前叶（AP）激素的非特异性释放作用。在6例患者中，静脉注射生长抑素（100微克推注+375微克静脉输注）完全消除了TRH（400微克静脉注射）诱导的GH升高；在12例患者中（其中7例对TRH有GH反应），LH-RH（100微克静脉注射）均未引起GH释放；4）最后，LH-RH（12例患者）未增加血浆催乳素（PRL），TRH（7例患者）未引起促性腺激素的非特异性释放。得出以下结论：1）对TRH的GH反应异常是肝硬化患者垂体前叶对下丘脑激素反应中唯一的改变；2）导致GH对TRH反应改变的机制与另一种病理状态即肢端肥大症中TRH诱导的GH升高的机制不同，在肢端肥大症中，TRH的作用不受生长抑素抑制，LH-RH可引起GH和PRL释放。
