Oi S, Ohi Y, Matsumoto S
No Shinkei Geka. 1977 Mar;5(3):223-8.
We have experienced with 50 cases of parasellar tumors, four cases of which had persistent thirst, polydipsia, polyuria, and reversible temporary hyponatremia secondary to hypernatriuresis. The mechanism of the syndrome in these four cases could not be explained by either that of the syndrome of hypernatremia or of the so-called SIADH. We tentatively named this syndrome as "CEREBRAL POLYURIC HYPONATREMIA" and the criteria of this syndrome as as follows: 1) persistent thirst, polydipsia polyuria, 2) reversible temporary hyponatremia secondary to hypernatriuresis, 3) exception of the following items--administration of uretic drugs, renal and adrenal dysfunction, hyperglycemia, hyperlipemia, overadministration of water, and poor administration of NaCl. The mechanism of this syndrome is presumed as follows: 1) compression by a tumor or surgical attack to the anterior hypothalamus, 2) disturbance of the mechanism of ADH secret-on, 3) extrasecretion of natriuretic factor possibly produced in the anterior hypthalamus, and 4) preservation of the thirst center.
我们对50例鞍旁肿瘤患者进行了观察,其中4例出现持续口渴、多饮、多尿以及继发于高钠血症的可逆性暂时性低钠血症。这4例患者综合征的机制既不能用高钠血症综合征来解释,也不能用所谓的抗利尿激素分泌异常综合征(SIADH)来解释。我们暂将此综合征命名为“脑性多尿性低钠血症”,该综合征的标准如下:1)持续口渴、多饮、多尿;2)继发于高钠血症的可逆性暂时性低钠血症;3)排除以下情况——使用利尿药、肾和肾上腺功能障碍、高血糖、高血脂、水摄入过多以及氯化钠摄入不足。该综合征的机制推测如下:1)肿瘤压迫或手术侵袭下丘脑前部;2)抗利尿激素分泌机制紊乱;3)可能由下丘脑前部产生的利钠因子分泌过多;4)口渴中枢保留。