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中枢性尿崩症患者的阿片类药物所致低钠血症:与抗利尿激素无关

Opioid-induced hyponatremia in a patient with central diabetes insipidus: independence from ADH.

作者信息

Bhat Nandini, Balliu Erjola, Osipoff Jennifer, Lane Andrew, Wilson Thomas

机构信息

.

出版信息

J Pediatr Endocrinol Metab. 2017 May 24;30(6):693-696. doi: 10.1515/jpem-2017-0001.

DOI:10.1515/jpem-2017-0001
PMID:28593907
Abstract

Hyponatremia can be a complication of opioid therapy, which has been postulated to occur secondary to inappropriate antidiuretic hormone secretion (syndrome of inappropriate antidiuretic hormone secretion [SIADH]). We report severe hyponatremia following wisdom teeth extraction with opioid analgesia in a 19-year-old female with diabetes insipidus (DI) and acquired panhypopituitarism that challenges this theory. As this patient has DI, we believe opioid treatment caused severe hyponatremia by the following mechanisms: (1) Opioids have a direct antidiuretic effect independent of changes in ADH, as demonstrated in Brattleboro rats with central DI. (2) Hydrocodone may have stimulated this patient's thirst center contributing to hyponatremia, as demonstrated in animal studies. Opioid use can cause hyponatremia in patients independent of ADH. It is important for clinicians to be aware of this so that patients can be appropriately counseled.

摘要

低钠血症可能是阿片类药物治疗的一种并发症,据推测其发生是由于抗利尿激素分泌不当(抗利尿激素分泌不当综合征[SIADH])。我们报告了一名19岁患有尿崩症(DI)和获得性全垂体功能减退的女性在拔除智齿并使用阿片类镇痛药后出现严重低钠血症,这对该理论提出了挑战。由于该患者患有尿崩症,我们认为阿片类药物治疗通过以下机制导致了严重低钠血症:(1)阿片类药物具有独立于抗利尿激素变化的直接抗利尿作用,如在患有中枢性尿崩症的布拉德福德大鼠中所证实的那样。(2)如动物研究所示,氢可酮可能刺激了该患者的口渴中枢,导致低钠血症。阿片类药物的使用可在不依赖抗利尿激素的情况下使患者发生低钠血症。临床医生了解这一点很重要,以便能够对患者进行适当的指导。

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