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精氨酸加压素过度释放是一种内分泌紊乱吗?病理生理学与治疗。

Is Exaggerated Release of Arginine Vasopressin an Endocrine Disorder? Pathophysiology and Treatment.

作者信息

Ishikawa San-E

机构信息

Department of Endocrinology and Metabolism, International University of Health and Welfare Hospital, Nasushiobara 329-2763, Tochigi, Japan.

出版信息

J Clin Med. 2017 Oct 31;6(11):102. doi: 10.3390/jcm6110102.

DOI:10.3390/jcm6110102
PMID:29088071
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5704119/
Abstract

Exaggerated release of arginine vasopressin (AVP) is profoundly involved in impaired water excretion and related hyponatremia. Such disorders underlie syndromes of inappropriate secretion of antidiuretic hormone (SIADH) and edematous diseases, such as congestive heart failure and decompensated liver cirrhosis. All the causes are fundamentally from non-endocrine diseases. AVP-induced water retention could produce hyponatremia, and further accelerate poor long-term outcome of edematous diseases. Administration of AVP V₂ receptor antagonists verifies how much AVP is involved in the pathogenesis of the impaired water excretion. The present paper demonstrated that exaggerated release of AVP plays a crucial role as an accessory endocrine disorder in pathological states of water retention and dilutional hyponatremia in non-endocrine disorders.

摘要

精氨酸加压素(AVP)的过度释放与水排泄受损及相关低钠血症密切相关。这些紊乱是抗利尿激素不适当分泌综合征(SIADH)和水肿性疾病(如充血性心力衰竭和失代偿期肝硬化)的基础。所有这些病因根本上都源于非内分泌疾病。AVP诱导的水潴留可导致低钠血症,并进一步加速水肿性疾病的不良长期预后。给予AVP V₂受体拮抗剂可验证AVP在水排泄受损的发病机制中所起的作用程度。本文表明,AVP的过度释放在非内分泌疾病导致水潴留和稀释性低钠血症的病理状态中作为一种辅助性内分泌紊乱发挥着关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d4b/5704119/12278ea88d7e/jcm-06-00102-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d4b/5704119/100b53f5e983/jcm-06-00102-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d4b/5704119/4a0bd6649e00/jcm-06-00102-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d4b/5704119/12278ea88d7e/jcm-06-00102-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d4b/5704119/100b53f5e983/jcm-06-00102-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d4b/5704119/4a0bd6649e00/jcm-06-00102-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1d4b/5704119/12278ea88d7e/jcm-06-00102-g003.jpg

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