Leal-Cerro A, Pumar A, Villamil F, Astorga R, Dieguez C, Casanueva F F
Department of Endocrinology, Hospital Virgen del Rocio, Sevilla, Spain.
Clin Endocrinol (Oxf). 1993 Apr;38(4):399-403. doi: 10.1111/j.1365-2265.1993.tb00521.x.
In patients with Cushing's syndrome, decreased growth hormone (GH) secretion is observed though the basic mechanism is unknown. In states of chronic deficiency of hypothalamic growth hormone releasing hormone (GHRH) release, a blunted GH response to exogenous GHRH has been reported; such impairment can be partially normalized by repetitive GHRH administration (priming). In order to clarify whether a deficit in hypothalamic release of GHRH is the basis of the decreased GH secretion in patients with Cushing's syndrome, GHRH plus pyridostigmine tests were undertaken, both before and after GHRH priming.
GHRH (200 micrograms/day as a single s.c. injection) was given daily over 7 days. Two pyridostigmine (120 mg p.o.) plus GHRH (100 micrograms i.v.) tests were performed before and after priming to assess GH response.
Eight patients (seven women, one man), with untreated Cushing's syndrome (six Cushing's disease, one autonomous bilateral adrenal hyperplasia, one adrenal adenoma), were studied.
Plasma GH levels were measured by immunoradiometric assay.
GHRH plus pyridostigmine-induced GH release was impaired in patients with untreated Cushing's syndrome (mean peak 5.2 +/- 1.4 mU/l, area under the curve (AUC) 472 +/- 96). Repetitive administration of GHRH over 7 days partially restored the GH response to the second pyridostigmine-GHRH test (mean peak 15.0 +/- 2.1 mU/l. AUC 1016 +/- 104), both P < 0.05. All of the eight Cushing's syndrome patients studied presented a higher GHRH plus pyridostigmine-induced GH secretion after priming.
Repetitive administration of GHRH increases the pyridostigmine-GHRH-induced GH secretion in patients with Cushing's syndrome. This suggests that impaired hypothalamic release of GHRH is a contributing factor to the decreased GH secretion observed in chronic hypercortisolism.
在库欣综合征患者中，观察到生长激素（GH）分泌减少，但其基本机制尚不清楚。在慢性下丘脑生长激素释放激素（GHRH）释放不足的状态下，已有报道对外源性GHRH的GH反应迟钝；这种损害可通过重复给予GHRH（预激）部分恢复正常。为了阐明下丘脑GHRH释放不足是否是库欣综合征患者GH分泌减少的基础，在GHRH预激前后均进行了GHRH加吡啶斯的明试验。
连续7天每天皮下注射一次GHRH（200微克/天）。在预激前后进行两次吡啶斯的明（口服120毫克）加GHRH（静脉注射100微克）试验，以评估GH反应。
研究了8例未经治疗的库欣综合征患者（7例女性，1例男性）（6例库欣病，1例自主性双侧肾上腺增生，1例肾上腺腺瘤）。
采用免疫放射分析法测定血浆GH水平。
未经治疗的库欣综合征患者中，GHRH加吡啶斯的明诱导的GH释放受损（平均峰值5.2±1.4 mU/l，曲线下面积（AUC）472±96）。连续7天重复给予GHRH部分恢复了对第二次吡啶斯的明-GHRH试验的GH反应（平均峰值15.0±2.1 mU/l，AUC 1016±104），两者P均<0.05。所研究的8例库欣综合征患者在预激后GHRH加吡啶斯的明诱导的GH分泌均较高。
重复给予GHRH可增加库欣综合征患者吡啶斯的明-GHRH诱导的GH分泌。这表明下丘脑GHRH释放受损是慢性高皮质醇血症中观察到的GH分泌减少的一个促成因素。
