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Brain metabolism in patients with hepatic encephalopathy studied by PET and MR
•Cerebral oxygen uptake and blood flow are reduced to 2/3 in cirrhotics with overt HE.•These two measures are not changed in cirrhotic patients with minimal HE or no HE.•Cerebral ammonia metabolism is enhanced due to increased blood ammonia in patients.•Cerebral ammonia kinetics is not affected by h...
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Published in: | Archives of biochemistry and biophysics 2013-08, Vol.536 (2), p.131-142 |
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description | •Cerebral oxygen uptake and blood flow are reduced to 2/3 in cirrhotics with overt HE.•These two measures are not changed in cirrhotic patients with minimal HE or no HE.•Cerebral ammonia metabolism is enhanced due to increased blood ammonia in patients.•Cerebral ammonia kinetics is not affected by hyperammonemia.•MR demonstrates low-grade cerebral white matter oedema in cirrhotics with HE.
We review PET- and MR studies on hepatic encephalopathy (HE) metabolism in human subjects from the point of views of methods, methodological assumptions and use in studies of cirrhotic patients with clinically overt HE, cirrhotic patients with minimal HE, cirrhotic patients with no history of HE and healthy subjects. Key results are: (1) Cerebral oxygen uptake and blood flow are reduced to 2/3 in cirrhotic patients with clinically overt HE but not in cirrhotic patients with minimal HE or no HE compared to healthy subjects. (2) Cerebral ammonia metabolism is enhanced due to increased blood ammonia in cirrhotic patients but the kinetics of cerebral ammonia uptake and metabolism is not affected by hyperammonemia. (3) Recent advantages in MR demonstrate low-grade cerebral oedema not only in astrocytes but also in the white matter in cirrhotic patients with HE. |
doi_str_mv | 10.1016/j.abb.2013.05.006 |
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We review PET- and MR studies on hepatic encephalopathy (HE) metabolism in human subjects from the point of views of methods, methodological assumptions and use in studies of cirrhotic patients with clinically overt HE, cirrhotic patients with minimal HE, cirrhotic patients with no history of HE and healthy subjects. Key results are: (1) Cerebral oxygen uptake and blood flow are reduced to 2/3 in cirrhotic patients with clinically overt HE but not in cirrhotic patients with minimal HE or no HE compared to healthy subjects. (2) Cerebral ammonia metabolism is enhanced due to increased blood ammonia in cirrhotic patients but the kinetics of cerebral ammonia uptake and metabolism is not affected by hyperammonemia. (3) Recent advantages in MR demonstrate low-grade cerebral oedema not only in astrocytes but also in the white matter in cirrhotic patients with HE.</description><identifier>ISSN: 0003-9861</identifier><identifier>EISSN: 1096-0384</identifier><identifier>DOI: 10.1016/j.abb.2013.05.006</identifier><identifier>PMID: 23726863</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>ammonia ; Ammonia - metabolism ; astrocytes ; blood ; blood flow ; brain ; Brain - blood supply ; Brain - metabolism ; Brain - pathology ; Brain Edema - metabolism ; Brain Edema - pathology ; Brain oedema ; Cerebral ammonia metabolism ; Cerebral blood flow ; Cerebral oxygen metabolism ; edema ; encephalopathy ; Hepatic Encephalopathy - complications ; Hepatic Encephalopathy - metabolism ; Hepatic Encephalopathy - pathology ; Humans ; Hyperammonemia ; Liver - metabolism ; Liver - pathology ; Liver Cirrhosis - complications ; Liver Cirrhosis - metabolism ; Liver Cirrhosis - pathology ; Magnetic Resonance Imaging - methods ; metabolism ; oxygen ; Oxygen - metabolism ; patients ; Positron-Emission Tomography - methods</subject><ispartof>Archives of biochemistry and biophysics, 2013-08, Vol.536 (2), p.131-142</ispartof><rights>2013 Elsevier Inc.</rights><rights>Copyright © 2013 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c377t-c3c840604c5e3b3e83b23568bd88bc47cc929ffb89a244b8878020b2a2619e8e3</citedby><cites>FETCH-LOGICAL-c377t-c3c840604c5e3b3e83b23568bd88bc47cc929ffb89a244b8878020b2a2619e8e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23726863$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Keiding, Susanne</creatorcontrib><creatorcontrib>Pavese, Nicola</creatorcontrib><title>Brain metabolism in patients with hepatic encephalopathy studied by PET and MR</title><title>Archives of biochemistry and biophysics</title><addtitle>Arch Biochem Biophys</addtitle><description>•Cerebral oxygen uptake and blood flow are reduced to 2/3 in cirrhotics with overt HE.•These two measures are not changed in cirrhotic patients with minimal HE or no HE.•Cerebral ammonia metabolism is enhanced due to increased blood ammonia in patients.•Cerebral ammonia kinetics is not affected by hyperammonemia.•MR demonstrates low-grade cerebral white matter oedema in cirrhotics with HE.
We review PET- and MR studies on hepatic encephalopathy (HE) metabolism in human subjects from the point of views of methods, methodological assumptions and use in studies of cirrhotic patients with clinically overt HE, cirrhotic patients with minimal HE, cirrhotic patients with no history of HE and healthy subjects. Key results are: (1) Cerebral oxygen uptake and blood flow are reduced to 2/3 in cirrhotic patients with clinically overt HE but not in cirrhotic patients with minimal HE or no HE compared to healthy subjects. (2) Cerebral ammonia metabolism is enhanced due to increased blood ammonia in cirrhotic patients but the kinetics of cerebral ammonia uptake and metabolism is not affected by hyperammonemia. (3) Recent advantages in MR demonstrate low-grade cerebral oedema not only in astrocytes but also in the white matter in cirrhotic patients with HE.</description><subject>ammonia</subject><subject>Ammonia - metabolism</subject><subject>astrocytes</subject><subject>blood</subject><subject>blood flow</subject><subject>brain</subject><subject>Brain - blood supply</subject><subject>Brain - metabolism</subject><subject>Brain - pathology</subject><subject>Brain Edema - metabolism</subject><subject>Brain Edema - pathology</subject><subject>Brain oedema</subject><subject>Cerebral ammonia metabolism</subject><subject>Cerebral blood flow</subject><subject>Cerebral oxygen metabolism</subject><subject>edema</subject><subject>encephalopathy</subject><subject>Hepatic Encephalopathy - complications</subject><subject>Hepatic Encephalopathy - metabolism</subject><subject>Hepatic Encephalopathy - pathology</subject><subject>Humans</subject><subject>Hyperammonemia</subject><subject>Liver - metabolism</subject><subject>Liver - pathology</subject><subject>Liver Cirrhosis - complications</subject><subject>Liver Cirrhosis - metabolism</subject><subject>Liver Cirrhosis - pathology</subject><subject>Magnetic Resonance Imaging - methods</subject><subject>metabolism</subject><subject>oxygen</subject><subject>Oxygen - metabolism</subject><subject>patients</subject><subject>Positron-Emission Tomography - methods</subject><issn>0003-9861</issn><issn>1096-0384</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNp9kE1PGzEQhq0KVALtD-gFfOwly9hee73iRCM-KvFRtXC2bO9s42g_gr1plX9fR4EeuczolZ55NXoI-cKgYMDU-aqwzhUcmChAFgDqA5kxqNUchC4PyAwAxLzWih2R45RWAIyVin8kR1xUXGklZuThW7RhoD1O1o1dSD3NaW2ngMOU6N8wLekSd9lTHDyul7Ybc1xuaZo2TcCGui39cfVE7dDQ-5-fyGFru4SfX_cJeb6-elrczu8eb74vLu_mXlTVlKfXJSgovUThBGrhuJBKu0Zr58vK-5rXbet0bXlZOq0rDRwct1yxGjWKE_J137uO48sG02T6kDx2nR1w3CTDSiZlXUvGM8r2qI9jShFbs46ht3FrGJidRrMyWaPZaTQgTdaYb05f6zeux-b_xZu3DJztgdaOxv6OIZnnX7lBAnAmVVVl4mJPYNbwJ2A0yYedwiZE9JNpxvDOA_8Avf6KgQ</recordid><startdate>20130815</startdate><enddate>20130815</enddate><creator>Keiding, Susanne</creator><creator>Pavese, Nicola</creator><general>Elsevier Inc</general><scope>FBQ</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20130815</creationdate><title>Brain metabolism in patients with hepatic encephalopathy studied by PET and MR</title><author>Keiding, Susanne ; Pavese, Nicola</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c377t-c3c840604c5e3b3e83b23568bd88bc47cc929ffb89a244b8878020b2a2619e8e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>ammonia</topic><topic>Ammonia - metabolism</topic><topic>astrocytes</topic><topic>blood</topic><topic>blood flow</topic><topic>brain</topic><topic>Brain - blood supply</topic><topic>Brain - metabolism</topic><topic>Brain - pathology</topic><topic>Brain Edema - metabolism</topic><topic>Brain Edema - pathology</topic><topic>Brain oedema</topic><topic>Cerebral ammonia metabolism</topic><topic>Cerebral blood flow</topic><topic>Cerebral oxygen metabolism</topic><topic>edema</topic><topic>encephalopathy</topic><topic>Hepatic Encephalopathy - complications</topic><topic>Hepatic Encephalopathy - metabolism</topic><topic>Hepatic Encephalopathy - pathology</topic><topic>Humans</topic><topic>Hyperammonemia</topic><topic>Liver - metabolism</topic><topic>Liver - pathology</topic><topic>Liver Cirrhosis - complications</topic><topic>Liver Cirrhosis - metabolism</topic><topic>Liver Cirrhosis - pathology</topic><topic>Magnetic Resonance Imaging - methods</topic><topic>metabolism</topic><topic>oxygen</topic><topic>Oxygen - metabolism</topic><topic>patients</topic><topic>Positron-Emission Tomography - methods</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Keiding, Susanne</creatorcontrib><creatorcontrib>Pavese, Nicola</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Archives of biochemistry and biophysics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Keiding, Susanne</au><au>Pavese, Nicola</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Brain metabolism in patients with hepatic encephalopathy studied by PET and MR</atitle><jtitle>Archives of biochemistry and biophysics</jtitle><addtitle>Arch Biochem Biophys</addtitle><date>2013-08-15</date><risdate>2013</risdate><volume>536</volume><issue>2</issue><spage>131</spage><epage>142</epage><pages>131-142</pages><issn>0003-9861</issn><eissn>1096-0384</eissn><abstract>•Cerebral oxygen uptake and blood flow are reduced to 2/3 in cirrhotics with overt HE.•These two measures are not changed in cirrhotic patients with minimal HE or no HE.•Cerebral ammonia metabolism is enhanced due to increased blood ammonia in patients.•Cerebral ammonia kinetics is not affected by hyperammonemia.•MR demonstrates low-grade cerebral white matter oedema in cirrhotics with HE.
We review PET- and MR studies on hepatic encephalopathy (HE) metabolism in human subjects from the point of views of methods, methodological assumptions and use in studies of cirrhotic patients with clinically overt HE, cirrhotic patients with minimal HE, cirrhotic patients with no history of HE and healthy subjects. Key results are: (1) Cerebral oxygen uptake and blood flow are reduced to 2/3 in cirrhotic patients with clinically overt HE but not in cirrhotic patients with minimal HE or no HE compared to healthy subjects. (2) Cerebral ammonia metabolism is enhanced due to increased blood ammonia in cirrhotic patients but the kinetics of cerebral ammonia uptake and metabolism is not affected by hyperammonemia. (3) Recent advantages in MR demonstrate low-grade cerebral oedema not only in astrocytes but also in the white matter in cirrhotic patients with HE.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>23726863</pmid><doi>10.1016/j.abb.2013.05.006</doi><tpages>12</tpages></addata></record> |
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subjects | ammonia Ammonia - metabolism astrocytes blood blood flow brain Brain - blood supply Brain - metabolism Brain - pathology Brain Edema - metabolism Brain Edema - pathology Brain oedema Cerebral ammonia metabolism Cerebral blood flow Cerebral oxygen metabolism edema encephalopathy Hepatic Encephalopathy - complications Hepatic Encephalopathy - metabolism Hepatic Encephalopathy - pathology Humans Hyperammonemia Liver - metabolism Liver - pathology Liver Cirrhosis - complications Liver Cirrhosis - metabolism Liver Cirrhosis - pathology Magnetic Resonance Imaging - methods metabolism oxygen Oxygen - metabolism patients Positron-Emission Tomography - methods |
title | Brain metabolism in patients with hepatic encephalopathy studied by PET and MR |
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