Imbriano Louis J, Grant Candace, Masani Naveed
NYU Grossman Long Island School of Medicine, 101 Mineola Blvd., Mineola, NY 11501, USA.
J Clin Med. 2024 Dec 27;14(1):92. doi: 10.3390/jcm14010092.
A knowledge gap may exist when attempting to identify the pathogenetic mechanisms resulting in the syndrome of inappropriate antidiuretic hormone (SIADH) or hypotonic hyponatremia. Ectopic secretion of antidiuretic hormone [ADH] is the classic cause of SIADH. But another form of inappropriate secretion of ADH occurs when interleukin 6 is activated. Hypotonic hyponatremia can also occur in patients with cerebral salt wasting, but the secretion of ADH is appropriate, responding to volume depletion induced by excessive natriuresis. Reset osmostat (RO) is another cause of hypotonic hyponatremia caused by an unknown anomaly in the hypothalamus. This review discusses the pathophysiology of and the identical laboratory findings found in classic ectopic ADH secretion, interleukin 6-mediated ADH secretion, cerebral salt wasting-induced ADH secretion, and RO. This review also discusses potential methods to discern which hypotonic hyponatremic syndrome is present and current recommendations for treatment.
在试图确定导致抗利尿激素分泌不当综合征（SIADH）或低渗性低钠血症的发病机制时，可能存在知识空白。抗利尿激素（ADH）的异位分泌是SIADH的经典病因。但当白细胞介素6被激活时，会出现另一种形式的ADH分泌不当。脑性盐耗综合征患者也可发生低渗性低钠血症，但其ADH分泌是适当的，对因过度利钠导致的容量耗竭作出反应。渗透压调定点重置（RO）是由下丘脑未知异常引起的低渗性低钠血症的另一个病因。本综述讨论了经典异位ADH分泌、白细胞介素6介导的ADH分泌、脑性盐耗引起的ADH分泌和RO的病理生理学及相同的实验室检查结果。本综述还讨论了辨别存在哪种低渗性低钠血症综合征的潜在方法以及当前的治疗建议。
