Trabert W, Caspari D, Bernhard P, Biro G
Department of Psychiatry, University of Saarland, Homburg/Saar, Germany.
Acta Psychiatr Scand. 1992 May;85(5):376-9. doi: 10.1111/j.1600-0447.1992.tb10322.x.
Forty-one male alcoholics suffering from alcohol withdrawal syndrome were investigated to assess the relationship between vasopressin (ADH), water homeostasis and alcohol withdrawal. During 10 d, we found a significant decrease in serum vasopressin, from 3.08 +/- 0.61 to 1.71 +/- 0.22 pg/nl. There were no concomitant changes in osmolality, so that a general dysregulatory state of vasopressin secretion during alcohol withdrawal cannot be assumed. Only patients with delirium tremens (8/41) had higher vasopressin levels despite lowered serum osmolalities. These findings support the hypothesis of an inappropriate rebound secretion of vasopressin in severe alcohol withdrawal. Furthermore, they may contribute to the pathogenesis of focal alcoholic brain damage, because rapid and/or profound changes in osmolality are suspected to cause circumscribed cerebral demyelinization.
对41名患有酒精戒断综合征的男性酗酒者进行了调查,以评估抗利尿激素(ADH)、水平衡与酒精戒断之间的关系。在10天内,我们发现血清抗利尿激素显著下降,从3.08±0.61皮克/纳升降至1.71±0.22皮克/纳升。渗透压没有相应变化,因此不能认为酒精戒断期间抗利尿激素分泌存在普遍的调节异常状态。只有震颤谵妄患者(8/41)尽管血清渗透压降低,但抗利尿激素水平较高。这些发现支持了严重酒精戒断时抗利尿激素不适当反弹分泌的假说。此外,它们可能有助于局灶性酒精性脑损伤的发病机制,因为渗透压的快速和/或深刻变化被怀疑会导致局限性脑脱髓鞘。