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神经性厌食症患者血浆和脑脊液中精氨酸加压素的异常。

Abnormalities in plasma and cerebrospinal-fluid arginine vasopressin in patients with anorexia nervosa.

作者信息

Gold P W, Kaye W, Robertson G L, Ebert M

出版信息

N Engl J Med. 1983 May 12;308(19):1117-23. doi: 10.1056/NEJM198305123081902.

DOI:10.1056/NEJM198305123081902
PMID:6835335
Abstract

Previous studies have indicated that many patients with anorexia nervosa have defects in urinary concentration or dilution suggestive of abnormal secretion of the antidiuretic hormone arginine vasopressin. To explore this possibility, we examined the response of plasma vasopressin to intravenous hypertonic saline in anorexic patients before and after correction of their weight loss. We also measured basal levels of the hormone in the cerebrospinal fluid. In all four subjects studied before correction of weight loss, the response to hypertonic saline was abnormal: in one, the plasma level of arginine vasopressin increased subnormally relative to the plasma sodium level; in the other three, it fluctuated erratically, with no relation to plasma sodium. These defects persisted in the three patients studied three to four weeks after recovery of body weight. In two patients who were initially studied when they were underweight, the defects were gone six months after recovery; in five of seven other patients studied at least six months after recovery but not while they were underweight, the response was normal. Abnormalities in the osmoregulation of plasma arginine vasopressin were not accounted for by nonosmotic stimuli and were almost always associated with an absolute increase in the level of arginine vasopressin in the cerebrospinal fluid or a reversal of the normal (less than 1.0) cerebrospinal fluid/plasma ratio of arginine vasopressin. These results indicate that most if not all patients with anorexia nervosa have abnormal levels of arginine vasopressin in their plasma and cerebrospinal fluid that are corrected very slowly with weight gain. The cause and consequences of these abnormalities remain to be determined.

摘要

以往的研究表明,许多神经性厌食症患者存在尿液浓缩或稀释功能缺陷,提示抗利尿激素精氨酸加压素分泌异常。为探究这种可能性,我们检测了厌食症患者体重减轻得到纠正前后,静脉注射高渗盐水后血浆加压素的反应。我们还测量了脑脊液中该激素的基础水平。在体重减轻得到纠正之前研究的所有4名受试者中,对高渗盐水的反应均异常:其中1名受试者,精氨酸加压素的血浆水平相对于血浆钠水平升高不足;在其他3名受试者中,其波动不稳定,与血浆钠无关。这些缺陷在体重恢复三至四周后研究的3名患者中持续存在。在最初体重过轻时进行研究的2名患者中,体重恢复6个月后缺陷消失;在恢复后至少6个月但体重未过轻时研究的其他7名患者中,有5名患者的反应正常。血浆精氨酸加压素的渗透调节异常并非由非渗透刺激引起,几乎总是与脑脊液中精氨酸加压素水平的绝对升高或脑脊液/血浆精氨酸加压素正常比值(小于1.0)的逆转相关。这些结果表明,大多数(如果不是全部)神经性厌食症患者血浆和脑脊液中的精氨酸加压素水平异常,体重增加后恢复非常缓慢。这些异常的原因和后果仍有待确定。

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