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容量依赖性抗利尿激素释放所致的下丘脑性高钠血症及其卡马西平和氯贝丁酯治疗

Hypothalamic hypernatremia due to volume--dependent ADH release, and its treatment with carbamazepine and clofibrate.

作者信息

Kimura T, Matsui K, Ota K, Yoshinaga K

出版信息

Tohoku J Exp Med. 1979 Feb;127(2):101-11. doi: 10.1620/tjem.127.101.

DOI:10.1620/tjem.127.101
PMID:760257
Abstract

A 23-year-old man, diagnosed as having a pituitary adenoma at the age of 17 and received an operation 1 month ago showed a fluctuating hypernatremia and hypodipsia. The water deprivation, water load and hypertonic saline infusion tests were carried out. After a 14-hr water deprivation test, plasma osmolality was 310 mOsm/kg, plasma ADH was 1.5 microunits/ml, and urine osmolality was 591 mOsm/kg. On the water load test subsequently performed, the plasma osmolality decreased to 297 mOsm/kg, but the urine was still hypertonic. Infusion of 2.5% saline solution elicited paradoxically a marked diuresis and dilution of urine despite the elevàtion of plasma osmolality. On the treatment with carbamazepine and clofibrate, the urinary osmolality increased, the hypernatremia was normalized, and a marked natriuresis was elicited with a gain in body weight. These results suggested that the secretion of ADH is regulated by changes in blood volume rather than by the plasma osmolality in this patient. The hypernatremia may be explained as a disturbance or lack of osmoreceptor function for ADH release and the loss of thirst sensation, though the volume receptor still remains functioning for ADH secretion. Depletion of the extracellular fluid volume may be another contributing factor to the elevation of serum sodium level by enhancing the reabsorption of sodium from renal tubules.

摘要

一名23岁男性,17岁时被诊断为垂体腺瘤,1个月前接受了手术,术后出现波动的高钠血症和低渗性多尿。进行了禁水试验、水负荷试验和高渗盐水输注试验。禁水14小时后,血浆渗透压为310 mOsm/kg,血浆抗利尿激素(ADH)为1.5微单位/毫升,尿渗透压为591 mOsm/kg。随后进行的水负荷试验中,血浆渗透压降至297 mOsm/kg,但尿液仍为高渗。输注2.5%盐水溶液时,尽管血浆渗透压升高,但却反常地引起明显利尿和尿液稀释。使用卡马西平和氯贝特治疗后,尿渗透压升高,高钠血症恢复正常,体重增加并出现明显利钠。这些结果表明,该患者ADH的分泌受血容量变化调节,而非血浆渗透压调节。高钠血症可解释为ADH释放的渗透压感受器功能紊乱或缺失以及口渴感觉丧失,尽管容量感受器仍能调节ADH分泌。细胞外液容量减少可能是通过增强肾小管对钠的重吸收导致血清钠水平升高的另一个因素。

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