Arginine Vasopressin and Posterior Reversible Encephalopathy Syndrome Pathophysiology: the Missing Link?

被引：0
作者：
Bérenger Largeau
Olivier Le Tilly
Bénédicte Sautenet
Charlotte Salmon Gandonnière
Chantal Barin-Le Guellec
Stephan Ehrmann
机构：
[1] CHRU de Tours,
[2] Laboratoire de Biochimie et Biologie Moléculaire,undefined
[3] Université de Tours,undefined
[4] Université de Nantes,undefined
[5] INSERM,undefined
[6] Methods in patients-centered outcomes and health research (SPHERE) - UMR 1246,undefined
[7] CHRU de Tours,undefined
[8] Service de Néphrologie-Hypertension artérielle,undefined
[9] Dialyses et Transplantation Rénale,undefined
[10] CHRU de Tours,undefined
[11] Service de Médecine Intensive Réanimation,undefined
[12] Université de Tours,undefined
[13] Université de Limoges,undefined
[14] INSERM,undefined
[15] Individual profiling and prevention of risks with immunosuppressive therapies and transplantation (IPPRITT) - UMR 1248,undefined
[16] CHRU de Tours,undefined
[17] Laboratoire de Biochimie et Biologie Moléculaire,undefined
[18] Université de Tours,undefined
[19] INSERM,undefined
[20] Centre d’étude des pathologies respiratoires (CEPR) - UMR 1100,undefined
[21] CHRU de Tours,undefined
[22] Service de Médecine Intensive Réanimation,undefined
[23] CIC 1415,undefined
[24] réseau CRICS-TRIGGERSEP,undefined
来源：
Molecular Neurobiology | 2019年 / 56卷
关键词：
Leukoencephalopathy syndrome; Hypertensive encephalopathy; Antidiuretic hormone; Neurological adverse drug reactions; Blood-brain barrier;
D O I：
暂无
中图分类号：
学科分类号：
摘要：
Posterior reversible encephalopathy syndrome (PRES) is a clinicoradiological entity characterized by a typical brain edema. Its pathogenesis is still debated through hypoperfusion and hyperperfusion theories, which have many limitations. As PRES occurs almost exclusively in clinical situations with arginine vasopressin (AVP) hypersecretion, such as eclampsia and sepsis, we hypothesize that AVP plays a central pathophysiologic role. In this review, we discuss the genesis of PRES and its symptoms through this novel approach. We theorize that AVP axis stimulation precipitates PRES development through an increase in AVP secretion or AVP receptor density. Activation of vasopressin V1a receptors leads to cerebral vasoconstriction, causing endothelial dysfunction and cerebral ischemia. This promotes cytotoxic edema through hydromineral transglial flux dysfunction and may increase endothelial permeability, leading to subsequent vasogenic brain edema. If our hypothesis is confirmed, it opens new perspectives for better patient monitoring and therapies targeting the AVP axis in PRES.
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页码：6792 / 6806
页数：14
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