Ambrosi B, Bochicchio D, Fadin C, Colombo P, Faglia G
Istituto di Scienze Endocrine, Università di Milano, Ospedale Maggiore IRCCS, Italy.
J Endocrinol Invest. 1990 Mar;13(3):257-61. doi: 10.1007/BF03349555.
Although somatostatin inhibits a variety of pituitary and non-pituitary hormones, not univocal data on its effects on ACTH release have been reported so far. In this study we investigated the effects of somatostatin or octreotide on ACTH levels of patients with corticotropin hypersecretion: 7 patients with Addison's disease, 2 patients previously adrenalectomized for Cushing's disease, 4 patients with Cushing's disease and 3 patients with ectopic ACTH syndrome. Plasma ACTH and cortisol levels were determined after somatostatin (500 micrograms over 60 min) infusion or octreotide (100 micrograms sc) injection. In 5 other patients with Cushing's disease ACTH and cortisol responses to CRH (1 microgram/kg iv) were evaluated in basal conditions and after octreotide acute administration. In no patients with Addison's disease any inhibitory influence of somatostatin (delta % = -21, -25) or octreotide (delta % = -38 +/- 12 vs -39 +/- 12 after saline) on plasma ACTH was found. Somatostatin did not significantly inhibit plasma ACTH in the two patients previously adrenalectomized for Cushing's disease and in 3 patients with Cushing's syndrome; in other 4 patients with Cushing's syndrome octreotide did not affect plasma ACTH levels. In 5 patients with Cushing's disease the plasma ACTH and cortisol responses to CRH were similar both before (ACTH from 9.9 +/- 1.7 pmol/L to 19.4 +/- 6.1 pmol/L; cortisol from 496 +/- 43.9 nmol/L to 923 +/- 355 nmol/L) and after octreotide injection (ACTH from 8.8 +/- 2.4 pmol/L to 19.1 +/- 8.2 pmol/L; cortisol from 510 +/- 54.6 nmol/L to 735 +/- 220 nmol/L). In conclusion, the acute administration of somatostatin or octreotide is not able to modify ACTH levels in patients with corticotropin hypersecretion either due to hypocortisolemic state or consequent to ACTH-secreting pituitary or ectopic tumors; moreover, octreotide does not affect the pituitary-adrenal responsiveness to CRH in patients with Cushing's disease.
尽管生长抑素可抑制多种垂体和非垂体激素，但迄今为止，关于其对促肾上腺皮质激素（ACTH）释放影响的数据并不一致。在本研究中，我们调查了生长抑素或奥曲肽对促肾上腺皮质激素分泌过多患者ACTH水平的影响：7例艾迪生病患者、2例因库欣病先前已行肾上腺切除术的患者、4例库欣病患者和3例异位ACTH综合征患者。在静脉输注生长抑素（60分钟内输注500微克）或皮下注射奥曲肽（100微克）后，测定血浆ACTH和皮质醇水平。在另外5例库欣病患者中，评估了基础状态下以及奥曲肽急性给药后ACTH和皮质醇对促肾上腺皮质激素释放激素（CRH，静脉注射1微克/千克）的反应。在艾迪生病患者中，未发现生长抑素（Δ% = -21，-25）或奥曲肽（与注射生理盐水后相比，Δ% = -38±12对-39±12）对血浆ACTH有任何抑制作用。生长抑素对2例因库欣病先前已行肾上腺切除术的患者以及3例库欣综合征患者的血浆ACTH无显著抑制作用；在另外4例库欣综合征患者中，奥曲肽未影响血浆ACTH水平。在5例库欣病患者中，注射奥曲肽前后，血浆ACTH和皮质醇对CRH的反应相似（ACTH从9.9±1.7皮摩尔/升升至19.4±6.1皮摩尔/升；皮质醇从496±43.9纳摩尔/升升至923±355纳摩尔/升）（注射奥曲肽后：ACTH从8.8±2.4皮摩尔/升升至19.1±8.2皮摩尔/升；皮质醇从510±54.6纳摩尔/升升至735±220纳摩尔/升）。总之，无论是由于皮质醇缺乏状态还是由于分泌ACTH的垂体或异位肿瘤导致促肾上腺皮质激素分泌过多的患者，急性给予生长抑素或奥曲肽均无法改变ACTH水平；此外，奥曲肽不影响库欣病患者垂体-肾上腺对CRH的反应性。
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