Main target of minimal hepatic encephalopathy: Morphophysiological, inflammatory and metabolic view

Arias, Natalia; Méndez, Marta; Gómez-Lázaro, Eneritz; Azpı́roz, Arantza; Árias, Jorge L.

doi:10.1016/j.physbeh.2015.06.019

Cited by 12 publications

(6 citation statements)

References 54 publications

(64 reference statements)

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“…37 GFAP expression has also been shown to be reduced during chronic liver disease and HE. 38,39 Loss of GFAP in chronic hepatitis was found to be related to astrocyte swelling, with subsequent loss of their stellate shape. 40 Similarly, in bile duct-ligated (BDL) rats, altered astrocytes have been found but with no changes in the total number of astrocytes themselves.…”

Section: Glial Fibrillary Acidic Protein (Gfap) and Oxidative Stressmentioning

confidence: 99%

The Direct Contribution of Astrocytes and Microglia to the Pathogenesis of Hepatic Encephalopathy

Jaeger

DeMorrow

McMillin

2019

Journal of Clinical and Translational Hepatology

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Hepatic encephalopathy is a neurological complication resulting from loss of hepatic function and is associated with poor clinical outcomes. During acute liver failure over 20% of mortality can be associated with the development of hepatic encephalopathy. In patients with liver cirrhosis, 1-year survival for those that develop overt hepatic encephalopathy is under 50%. The pathogenesis of hepatic encephalopathy is complicated due to the multiple disruptions in homeostasis that occur following a reduction in liver function. Of these, elevations of ammonia and neuroinflammation have been shown to play a significant contributing role to the development of hepatic encephalopathy. Disruption of the urea cycle following liver dysfunction leads to elevations of circulating ammonia, which enter the brain and disrupt the functioning of astrocytes. This results in dysregulation of metabolic pathways in astrocytes, oxidative stress and cerebral edema. Besides ammonia, circulating chemokines and cytokines are increased following liver injury, leading to activation of microglia and a subsequent neuroinflammatory response. The combination of astrocyte dysfunction and microglia activation are significant contributing factors to the pathogenesis of hepatic encephalopathy.

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Section: Glial Fibrillary Acidic Protein (Gfap) and Oxidative Stressmentioning

confidence: 99%

The Direct Contribution of Astrocytes and Microglia to the Pathogenesis of Hepatic Encephalopathy

Jaeger

DeMorrow

McMillin

2019

Journal of Clinical and Translational Hepatology

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“…3). This gut-brain impact has been supported by Arias et al, 25,26 who demonstrated that animals with pre-hepatic portal hypertension showed decreased metabolic brain consumption, along with lower density of astrocytes and an increase in the tumor necrotic factor-α in specific brain regions. Moreover, pre-hepatic portal hypertensive animals showed changes in the neuronal nuclear volume across the brain, underlying the cognitive deficits found in experimental models and patients.…”

Section: Mechanotransduction In Pre-hepatic Portal Hypertension: a Mumentioning

confidence: 74%

Hepatic encephalopathy: Sometimes more portal than hepatic

Aller

Arias

Blanco-Rivero

et al. 2018

J of Gastro and Hepatol

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Hepatic encephalopathy is a severe complication of both chronic and acute liver diseases. The term hepatic encephalopathy stems from the belief that hepatic insufficiency is its fundamental etiopathogenic factor. However, most clinical cases show liver failure along with mesenteric venous portal hypertension. This portal hypertension would explain the abnormal mechanical forces suffered by the digestive tract in the early stages of the disorder. These forces could regulate some gut biochemical pathological pathways in a process known as mechanotransduction. Thus, portal hypertension would begin with the establishment of a mechanotransduced afferent or sensory inflammatory gut‐brain pathway, resulting in functional and structural changes in the central nervous system. In this review, we will revisit the term “hepatic encephalopathy” in light of new results where portal hypertension occurs before liver failure and is accompanied by brain changes. Moreover, we will point out cellular links that can explain the microbiota, immune, gut, and brain axis disturbances found in this disorder.

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“…It has been suggested that FD reductions may result from brain inflammatory-related processes (e.g., inflammatory infiltration, loss of cell shape, necrosis, or irregular 3 Neural Plasticity tissue organization) [33]. Previous studies have persistently reported the activation of microglia cells, increased inflammatory factor levels (e.g., TNF, IL-6, and IL-1β) [34,35], Alzheimer's type II astrocytosis [36,37], and neuronal cell death [38] in patients with liver failure. Therefore, it is expected that cirrhotic patients with MHE showed reduced fractal dimension in multiple brain regions.…”

Section: Discussionmentioning

confidence: 99%

Reduced Cortical Complexity in Cirrhotic Patients with Minimal Hepatic Encephalopathy

et al. 2020

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Purpose. Gray matter volume loss, regional cortical thinning, and local gyrification index alteration have been documented in minimal hepatic encephalopathy (MHE). Fractal dimension (FD), another morphological parameter, has been widely used to describe structural complexity alterations in neurological or psychiatric disease. Here, we conducted the first study to investigate FD alterations in MHE. Methods and Materials. We performed high-resolution structural magnetic resonance imaging on cirrhotic patients with MHE (n=20) and healthy controls (n=21). We evaluated their cognitive performance using the psychometric hepatic encephalopathy score (PHES). The regional FD value was calculated by Computational Anatomy Toolbox (CAT12) and compared between groups. We further estimated the association between patients’ cognitive performance and FD values. Results. MHE patients presented significantly decreased FD values in the left precuneus, left supramarginal gyrus, right caudal anterior cingulate cortex, right isthmus cingulate cortex, right insula, bilateral pericalcarine cortex, and bilateral paracentral cortex compared to normal controls. In addition, the FD values in the right isthmus cingulate cortex and right insula were shown to be positively correlated with patients’ cognitive performance. Conclusion. Aberrant cortical complexity is an additional characteristic of MHE, and FD analysis may provide novel insight into the neurobiological basis of cognitive dysfunction in MHE.

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Main target of minimal hepatic encephalopathy: Morphophysiological, inflammatory and metabolic view

Cited by 12 publications

References 54 publications

The Direct Contribution of Astrocytes and Microglia to the Pathogenesis of Hepatic Encephalopathy

The Direct Contribution of Astrocytes and Microglia to the Pathogenesis of Hepatic Encephalopathy

Hepatic encephalopathy: Sometimes more portal than hepatic

Reduced Cortical Complexity in Cirrhotic Patients with Minimal Hepatic Encephalopathy

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