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Hepatic Encephalopathy

Hepatic encephalopathy (HE) is a brain disorder caused by chronic liver failure, particularly in alcoholics with cirrhosis, which results in cognitive, psychiatric, and motor impairments. In these patients, the number of functional liver cells is reduced, and some blood is diverted around the liver...

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Autor principal: Butterworth, Roger F.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: National Institute on Alcohol Abuse and Alcoholism 2003
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6668878/
https://www.ncbi.nlm.nih.gov/pubmed/15535452
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author Butterworth, Roger F.
author_facet Butterworth, Roger F.
author_sort Butterworth, Roger F.
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description Hepatic encephalopathy (HE) is a brain disorder caused by chronic liver failure, particularly in alcoholics with cirrhosis, which results in cognitive, psychiatric, and motor impairments. In these patients, the number of functional liver cells is reduced, and some blood is diverted around the liver before toxins are removed. As a result, toxins such as ammonia and manganese can accumulate in the blood and enter the brain, where they can damage nerve cells and supporting cells called astrocytes. Positron emission tomography analyses have determined that ammonia levels are elevated in the brains of HE patients; ammonia accumulation can alter the expression of various important brain genes. Magnetic resonance images show that manganese is deposited in a brain area called the globus pallidus; manganese deposits may be responsible for structural changes in the astrocytes that are characteristic of HE. Treatment of patients with HE involves measures to lower ammonia levels in the blood, medications to counteract ammonia’s effects on brain cell function, devices to compensate for liver dysfunction, and liver transplantation.
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spelling pubmed-66688782019-08-05 Hepatic Encephalopathy Butterworth, Roger F. Alcohol Res Health Articles Hepatic encephalopathy (HE) is a brain disorder caused by chronic liver failure, particularly in alcoholics with cirrhosis, which results in cognitive, psychiatric, and motor impairments. In these patients, the number of functional liver cells is reduced, and some blood is diverted around the liver before toxins are removed. As a result, toxins such as ammonia and manganese can accumulate in the blood and enter the brain, where they can damage nerve cells and supporting cells called astrocytes. Positron emission tomography analyses have determined that ammonia levels are elevated in the brains of HE patients; ammonia accumulation can alter the expression of various important brain genes. Magnetic resonance images show that manganese is deposited in a brain area called the globus pallidus; manganese deposits may be responsible for structural changes in the astrocytes that are characteristic of HE. Treatment of patients with HE involves measures to lower ammonia levels in the blood, medications to counteract ammonia’s effects on brain cell function, devices to compensate for liver dysfunction, and liver transplantation. National Institute on Alcohol Abuse and Alcoholism 2003 /pmc/articles/PMC6668878/ /pubmed/15535452 Text en http://creativecommons.org/publicdomain/mark/1.0/ Unless otherwise noted in the text, all material appearing in this journal is in the public domain and may be reproduced without permission. Citation of the source is appreciated.
spellingShingle Articles
Butterworth, Roger F.
Hepatic Encephalopathy
title Hepatic Encephalopathy
title_full Hepatic Encephalopathy
title_fullStr Hepatic Encephalopathy
title_full_unstemmed Hepatic Encephalopathy
title_short Hepatic Encephalopathy
title_sort hepatic encephalopathy
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6668878/
https://www.ncbi.nlm.nih.gov/pubmed/15535452
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