Iwasaki Y, Kondo K, Hasegawa H, Oiso Y
First Department of Internal Medicine, Nagoya University School of Medicine, Japan.
Horm Res. 1997;47(1):38-44. doi: 10.1159/000185368.
Neurohypophyseal function was studied by hypertonic saline infusion with plasma vasopressin measurement in 3 patients with adrenal insufficiency before and after cortisol replacement. Although each patient had different causes of adrenal insufficiency, all showed impaired water excretion before replacement. The first patient with isolated adrenocorticotropin deficiency had marked hyponatremia and inappropriate vasopressin secretion which was normalized after replacement, indicating vasopressin hypersecretion during hypoadrenocorticism. The second patient had combined anterior and posterior pituitary deficiency due to postpartum hypopituitarism and showed completely absent vasopressin secretion, with her polyuria being masked before cortisol replacement, suggesting a vasopressin-independent intrarenal mechanism of antidiuresis. The third patient with panhypopituitarism due to a pituitary tumor also had preexisting diabetes insipidus with defective vasopressin secretion. In this case, however, plasma vasopressin was found to be elevated when adrenal insufficiency and hyponatremia subsequently developed. Together, these results indicate that vasopressin hypersecretion does occur during adrenal insufficiency, but that the accompanying urinary diluting defect may be attributable either to vasopressin-dependent or to vasopressin-independent mechanisms.
通过对3例肾上腺功能不全患者在皮质醇替代治疗前后进行高渗盐水输注并测定血浆血管加压素，研究了神经垂体功能。尽管每位患者肾上腺功能不全的病因不同，但在替代治疗前均表现出排水功能受损。首例单纯促肾上腺皮质激素缺乏患者有明显低钠血症和不适当的血管加压素分泌，替代治疗后恢复正常，提示肾上腺皮质功能减退期间血管加压素分泌过多。第二例患者因产后垂体功能减退导致垂体前叶和后叶联合功能减退，血管加压素分泌完全缺失，其多尿在皮质醇替代治疗前被掩盖，提示存在不依赖血管加压素的肾内抗利尿机制。第三例因垂体肿瘤导致全垂体功能减退的患者既往也有尿崩症，血管加压素分泌存在缺陷。然而，在该病例中，当随后出现肾上腺功能不全和低钠血症时，发现血浆血管加压素升高。总之，这些结果表明肾上腺功能不全期间确实会发生血管加压素分泌过多，但伴随的尿液稀释缺陷可能归因于依赖血管加压素或不依赖血管加压素的机制。
