Modification in CSF specific gravity in acutely decompensated cirrhosis and acute on chronic liver failure independent of encephalopathy, evidences for an early blood-CSF barrier dysfunction in cirrhosis

Weiss, Nicolas; Rosselli, Matteo; Mouri, Sarah; Galanaud, Damien; Puybasset, Louis; Agarwal, Banwari; Thabut, Dominique; Jalan, Rajiv

doi:10.1007/s11011-016-9916-9

Cited by 22 publications

(22 citation statements)

References 37 publications

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“…One of the clinical features thought to contribute to the pathogenesis of hepatic encephalopathy is an increased permeability of the blood-brain barrier to a number of solutes that is not attributable to a general breakdown in the integrity of the blood-brain barrier. 28,29 Permeability of the blood-brain barrier, as demonstrated by Evans blue extravasation, occurs as a later event well after the onset of neurological symptoms in various rodent models of acute liver failure. [30][31][32] Furthermore, the increased permeability of the blood-brain barrier seems to be dependent upon the presence of pro-inflammatory factors.…”

Section: Effect Of Bile Acids On Blood-brain Barrier Permeabilitymentioning

confidence: 99%

Bile Acids in Hepatic Encephalopathy

DeMorrow

2019

Journal of Clinical and Experimental Hepatology

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TX 76504, USA and y Central Texas Veterans Healthcare System, Temple, TX 76504, USA Hepatic encephalopathy describes the array of neurological complications that arise due to liver insufficiency and/or portal-systemic shunt. The pathogenesis of hepatic encephalopathy shares a longstanding association with hyperammonemia and inflammation. Recently, aberrant bile acid signaling has been implicated in the development of key features of hepatic encephalopathy due to acute liver failure including neuronal dysfunction, neuroinflammation and blood-brain barrier permeability. This review summarizes the findings of recent studies demonstrating a role for bile acids in hepatic encephalopathy and speculates on the possible downstream consequences of bile acid signaling. ( J CLIN EXP HEPATOL 2019;9:117-124) Keywords: blood-brain barrier, farnesoid X receptor, neuroinflammation, sphingosine-1-phosphate receptor 2, Takeda G-protein coupled receptor 5 (TGR5)

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Section: Effect Of Bile Acids On Blood-brain Barrier Permeabilitymentioning

confidence: 99%

Bile Acids in Hepatic Encephalopathy

DeMorrow

2019

Journal of Clinical and Experimental Hepatology

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“…In cirrhosis, the glutamine increase is gradual and astrocytes respond by progressively extruding intracytoplasmic myoinositol and taurine to try and maintain osmotic equilibrium. This largely explains why brain edema is rarely present in cirrhosis and/or in acute on chronic liver failure (ACLF) [6,7]. In neurons, glutamine is deaminated into glutamate, the most important excitatory neurotransmitter in the brain, that stimulates neurons [8].…”

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confidence: 99%

Understanding hepatic encephalopathy

2017

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“…We identi ed post-resuscitation shock as factor associated with having nonspeci c CSF abnormalities. The systemic in ammation seen in post-resuscitation shock may cause BBB alterations, as described in acute sepsis and cirrhosis, [25,26]. Moreover, patients presenting with confusion to coma before CA and who demonstrated oedema on cerebral CT Scan were more likely to have nonspeci c CSF abnormalities.…”

Section: Discussionmentioning

confidence: 99%

Diagnostic and Prognostic Contribution of Cerebrospinal Fluid Analysis After Cardiac Arrest

Paul¹,

Benghanem²,

Merceron³

et al. 2020

Preprint

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Background: Lumbar puncture is among the investigations used to determine the aetiology and prognosis of cardiac arrest, despite a dearth of data on its performance. We aimed to assess the diagnostic and prognostic performance of lumbar puncture after cardiac arrest. Methods: We retrospectively studied data from prospectively established databases of consecutive patients who were admitted to two French ICUs in 2007-2016 with sustained return of spontaneous circulation (ROSC) after cardiac arrest and who underwent lumbar puncture as an aetiological investigation. Results: Of 1984 patients with sustained ROSC, 65 (3.3%) underwent lumbar puncture and were included. Lumbar puncture identified a neurological cause of cardiac arrest in 6/65 (9%) patients, including 5 with neurologic prodromal symptoms before cardiac arrest and 4 with the lumbar puncture done post-mortem. Lumbar puncture performed before death showed nonspecific cerebrospinal fluid abnormalities in 37/53 (69.8%) patients. By univariate analysis, factors significantly associated with cerebrospinal fluid abnormalities were shorter no-flow time (0 min [0-3] versus 4 min [2-10], p=0.004) and post-resuscitation shock (26 [70%] versus 5 [31%], p<0.01). Presence of cerebrospinal fluid abnormalities was non significantly associated with poorer outcomes (CPC 3-4-5) (p=0.06). Conclusions: Lumbar puncture, although rarely performed, can contribute to the aetiological diagnosis of cardiac arrest. As a second-line investigation, it identified the cause in 9% of our patients. Nonspecific cerebrospinal fluid abnormalities are common after cardiac arrest, perhaps due to blood-brain barrier disruption, and may carry prognostic significance.

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Modification in CSF specific gravity in acutely decompensated cirrhosis and acute on chronic liver failure independent of encephalopathy, evidences for an early blood-CSF barrier dysfunction in cirrhosis

Abstract: Introduction: Although hepatic encephalopathy (HE) on the background of acute on

Cited by 22 publications

References 37 publications

Bile Acids in Hepatic Encephalopathy

Bile Acids in Hepatic Encephalopathy

Understanding hepatic encephalopathy

Diagnostic and Prognostic Contribution of Cerebrospinal Fluid Analysis After Cardiac Arrest

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