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

Largeau, Bérenger; Tilly, Olivier Le; Sautenet, Bénédicte; Gandonnière, Charlotte Salmon; Guellec, Chantal Barin‐Le; Ehrmann, Stéphan

doi:10.1007/s12035-019-1553-y

Cited by 34 publications

(51 citation statements)

References 113 publications

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“…It has been demonstrated that AVP is released as a response to peripheral inflammation and in brain injury AVP secretion also increases [21][22][23][24][25] . During brain injury AVP leads to cerebral vessel constriction and increased sympathetic tone, ensuing endothelial dysfunction and cerebral ischemia 26,27 .…”

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confidence: 99%

“…AVP also promotes dysregulation of ionic-water flux in the BBB through astrocytic Na + / K + ATPase, Na-K-Cl cotransporter (NKCC), and Aquaporin-4 (AQP-4) dysfunction 11,[28][29][30] , resulting in cytotoxic edema 30 . Brain ischemia can trigger vascular endothelial growth factor (VEGF) overexpression and increase endothelial permeability through AVP positive feedback 24 . On the other hand, the use of V1a and V2 receptor blockers, as conivaptan, in brain injury has been extensively reported; in fact, conivaptan reduces brain edema and BBB disruption during brain ischemia and cardiac arrest in mice 10,12 .…”

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confidence: 99%

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Blockade of Arginine Vasopressin receptors prevents blood-brain barrier breakdown in Experimental Autoimmune Encephalomyelitis

Viñuela-Berni

Gómez-González

Quintanar‐Stephano

2020

Sci Rep

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The blood-brain barrier (BBB) plays a significant pathophysiological role in multiple sclerosis (MS). Vasopressin (AVP) is released after brain injury and contributes to the inflammatory response. We propose that AVP may be modulating BBB permeability and hence affecting EAE clinical signs. Female Lewis rats were immunized s.c. with guinea-pig brain extract suspended in complete Freund's adjuvant. prior to that, animals were subjected to neurointermediate pituitary lobectomy (niL) or treated with AVP receptor antagonist (conivaptan). BBB permeability assays were performed. Western blot for claudin-5 and histological analysis were performed in conivaptan treated EAE rats. EAE increase in BBB permeability to Evans blue was reverted by the NIL surgery. AVP receptor blockade reverted the EAE BBB hyperpermeability to Evans blue and 10-kDa FITC-dextran in almost all brain regions. Both, AVP low levels and AVP receptor blockade attenuated EAE clinical signs. Conivaptan reduced perivascular cuffs in EAE rats. A decrease in claudin-5 expression was observed in EAE rats and conivaptan treatment partially restored normal levels. Our data indicate that V1a and V2 AVP receptors can modulate BBB permeability and consequently are involved in the CNS inflammatory process during EAE. Future research is required to characterize the utility of vasopressin antagonist in MS treatment.

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confidence: 99%

mentioning

confidence: 99%

Blockade of Arginine Vasopressin receptors prevents blood-brain barrier breakdown in Experimental Autoimmune Encephalomyelitis

Viñuela-Berni

Gómez-González

Quintanar‐Stephano

2020

Sci Rep

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“…She was administered with oral nimodipine 360 mg/day because of the neuroprotective effect of this drug (5,6). She left the hospital 48 h later with continuation of nimodipine at home and was followed up by ambulatory care as an outpatient.…”

Section: Therapeutic Interventionsmentioning

confidence: 99%

“…According to this novel theory, cytotoxic edema is induced by a transglial flux dysfunction with enhanced endothelial permeability, generating vasogenic brain edema. AVP can mediate also endothelial dysfunction through hypersecretion of vascular endothelial growth factor (VEGF) (6).…”

Section: Pathophysiology the Theories To Explain Posterior Reversiblementioning

confidence: 99%

“…A study published by Liman and colleagues showed that patients with PRES who have received chemotherapy or immunosuppressive medication show significantly lower mean arterial pressure than did those with PRES from other etiologies (25). Platinum salts are a well-known trigger of AVP hypersecretion (6), and they have a direct toxic effect on endothelial cells (26,27). 5-Fluorouracil can cause a direct neurotoxic effect through the interruption of Krebs cycle or through thiamine deficiency (28,29); a neurotoxic effect is reported also in case of dihydropyrimidine dehydrogenase (DPD), the initial and ratelimiting enzyme in the catabolism of fluoropyrimidines (30,31).…”

Section: Chemotherapy and Pres: What Does Our Case Add To The Literatmentioning

confidence: 99%

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Delayed Posterior Reversible Leukoencephalopathy Syndrome Triggered by FLOT Chemotherapy

2020

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Posterior reversible encephalopathy syndrome (PRES) is a potentially severe disorder of the autoregulation of cerebral perfusion. The major clinical manifestations are headache, seizures, altered mental status, and visual loss. The typical radiological finding is vasogenic edema predominating in the white matter of occipital and parietal lobes. PRES is increasingly recognized as a clinico-radiological entity owing to improvements and fast availability of brain imaging, especially magnetic resonance imaging (MRI). We present the exceptional case of a 67-year-old female patient with a gastric adenocarcinoma at stage IIB (T3N0M0) treated by FLOT chemotherapy (5-fluorouracil, oxaliplatin, docetaxel, and folinic acid). Two months after the unique administration of FLOT regimen, she developed sudden posterior headache and visual loss. Blood pressure values were normal. Cerebral tomography showed ischemic-like occipital bilateral lesions, and angiographic sequences revealed breakdown of the blood-brain barrier (BBB). MRI revealed bilateral parieto-occipital T1 hypointensity and T2 hyperintensity, which demonstrated vasogenic edema. The rest of the parts of the lesions were T1 hyperintensity, T2 hyperintensity, and diffusion-weighted imaging (DWI) hyperintensity, which indicate cortical laminar necrosis. After injection of gadolinium, a linear enhancement of the cortex was observed. She was treated with oral nimodipine. Follow-up was characterized by permanent visual sequelae and tetraparesis. PRES represents an urgent neurological condition. Our observation highlights that PRES should be considered in patients under chemotherapy, even when their blood pressure remains within normal range. This is the first report of PRES triggered by FLOT chemotherapy and with a silent window of 2 months between chemotherapy and PRES, widening further the spectrum of chemotherapy-induced PRES. Our case highlights the potential role of FLOT regimen in the pathogenesis of PRES and the need for a novel approach in terms of prevention of this potentially fatal complication when patients receive chemotherapy.

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Coexisting posterior reversible encephalopathy syndrome and ischemic hepatopathy: A case report

Adetoye

Baumgartner

Rajkotia

et al. 2021

Clinical Case Reports

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

Cited by 34 publications

References 113 publications

Blockade of Arginine Vasopressin receptors prevents blood-brain barrier breakdown in Experimental Autoimmune Encephalomyelitis

Blockade of Arginine Vasopressin receptors prevents blood-brain barrier breakdown in Experimental Autoimmune Encephalomyelitis

Delayed Posterior Reversible Leukoencephalopathy Syndrome Triggered by FLOT Chemotherapy

Coexisting posterior reversible encephalopathy syndrome and ischemic hepatopathy: A case report

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