Systemic inflammatory response exacerbates the neuropsychological effects of induced hyperammonemia in cirrhosis
Studies in acute liver failure show correlation between evidence of a systemic inflammatory response syndrome (SIRS) and progression of hepatic encephalopathy (HE). We tested the hypothesis that SIRS mediators, such as nitric oxide and proinflammatory cytokines, may exacerbate the neuropsychological...
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| Veröffentlicht in: | Journal of hepatology 2004-02, Vol.40 (2), p.247-254 |
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| creator | Shawcross, Debbie L Davies, Nathan A Williams, Roger Jalan, Rajiv |
| description | Studies in acute liver failure show correlation between evidence of a systemic inflammatory response syndrome (SIRS) and progression of hepatic encephalopathy (HE). We tested the hypothesis that SIRS mediators, such as nitric oxide and proinflammatory cytokines, may exacerbate the neuropsychological effects of hyperammonemia in cirrhosis.
Ten patients with cirrhosis were studied, 24–36 h after admission with clinical evidence of infection, and following its resolution. Hyperammonemia was induced by oral administration of an amino-acid (aa) solution mimicking hemoglobin composition. Inflammatory mediators, nitrate/nitrite, ammonia, aa profiles and a battery of neuropsychological tests were measured.
The hyperammonemia generated in response to the aa solution was similar prior to, and after resolution, of the inflammation (P=0.77). With treatment of the infection there were significant reductions in white blood cell count (WBC), C-reactive protein (CRP), nitrate/nitrite, interleukin-6, interleukin-1β and tumour necrosis factor α. Induced hyperammonemia resulted in significant worsening of the neuropsychological scores when patients showed evidence of SIRS but not after its resolution.
The significant deterioration of neuropsychological test scores following induced hyperammonemia during the inflammatory state, but not after its resolution, suggests that the inflammation and its mediators may be important in modulating the cerebral effect of ammonia in liver disease. |
| doi_str_mv | 10.1016/j.jhep.2003.10.016 |
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Ten patients with cirrhosis were studied, 24–36 h after admission with clinical evidence of infection, and following its resolution. Hyperammonemia was induced by oral administration of an amino-acid (aa) solution mimicking hemoglobin composition. Inflammatory mediators, nitrate/nitrite, ammonia, aa profiles and a battery of neuropsychological tests were measured.
The hyperammonemia generated in response to the aa solution was similar prior to, and after resolution, of the inflammation (P=0.77). With treatment of the infection there were significant reductions in white blood cell count (WBC), C-reactive protein (CRP), nitrate/nitrite, interleukin-6, interleukin-1β and tumour necrosis factor α. Induced hyperammonemia resulted in significant worsening of the neuropsychological scores when patients showed evidence of SIRS but not after its resolution.
The significant deterioration of neuropsychological test scores following induced hyperammonemia during the inflammatory state, but not after its resolution, suggests that the inflammation and its mediators may be important in modulating the cerebral effect of ammonia in liver disease.</description><identifier>ISSN: 0168-8278</identifier><identifier>EISSN: 1600-0641</identifier><identifier>DOI: 10.1016/j.jhep.2003.10.016</identifier><identifier>PMID: 14739095</identifier><identifier>CODEN: JOHEEC</identifier><language>eng</language><publisher>Oxford: Elsevier B.V</publisher><subject>Amino Acids - blood ; Amino-acid solution ; Aminoacid disorders ; Ammonia - blood ; Biological and medical sciences ; C-Reactive Protein - metabolism ; Errors of metabolism ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Hepatic Encephalopathy - complications ; Hepatic Encephalopathy - immunology ; Hepatic Encephalopathy - psychology ; Humans ; Hyperammonemia - complications ; Hyperammonemia - immunology ; Hyperammonemia - psychology ; Inflammation - complications ; Inflammation - immunology ; Inflammation - psychology ; Inflammation Mediators - metabolism ; Liver Cirrhosis - complications ; Liver Cirrhosis - immunology ; Liver Cirrhosis - psychology ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Mental Recall ; Metabolic diseases ; Middle Aged ; Minimal hepatic encephalopathy ; Neuropsychological function ; Neuropsychological Tests ; Other diseases. Semiology ; Proinflammatory cytokines ; Reaction Time</subject><ispartof>Journal of hepatology, 2004-02, Vol.40 (2), p.247-254</ispartof><rights>2003 European Association for the Study of the Liver</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c492t-111146b488d6dd677a42d4caef48ad4a5bb6df58df3b3f31adeaee8d6bac900f3</citedby><cites>FETCH-LOGICAL-c492t-111146b488d6dd677a42d4caef48ad4a5bb6df58df3b3f31adeaee8d6bac900f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.jhep.2003.10.016$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15481017$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14739095$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shawcross, Debbie L</creatorcontrib><creatorcontrib>Davies, Nathan A</creatorcontrib><creatorcontrib>Williams, Roger</creatorcontrib><creatorcontrib>Jalan, Rajiv</creatorcontrib><title>Systemic inflammatory response exacerbates the neuropsychological effects of induced hyperammonemia in cirrhosis</title><title>Journal of hepatology</title><addtitle>J Hepatol</addtitle><description>Studies in acute liver failure show correlation between evidence of a systemic inflammatory response syndrome (SIRS) and progression of hepatic encephalopathy (HE). We tested the hypothesis that SIRS mediators, such as nitric oxide and proinflammatory cytokines, may exacerbate the neuropsychological effects of hyperammonemia in cirrhosis.
Ten patients with cirrhosis were studied, 24–36 h after admission with clinical evidence of infection, and following its resolution. Hyperammonemia was induced by oral administration of an amino-acid (aa) solution mimicking hemoglobin composition. Inflammatory mediators, nitrate/nitrite, ammonia, aa profiles and a battery of neuropsychological tests were measured.
The hyperammonemia generated in response to the aa solution was similar prior to, and after resolution, of the inflammation (P=0.77). With treatment of the infection there were significant reductions in white blood cell count (WBC), C-reactive protein (CRP), nitrate/nitrite, interleukin-6, interleukin-1β and tumour necrosis factor α. Induced hyperammonemia resulted in significant worsening of the neuropsychological scores when patients showed evidence of SIRS but not after its resolution.
The significant deterioration of neuropsychological test scores following induced hyperammonemia during the inflammatory state, but not after its resolution, suggests that the inflammation and its mediators may be important in modulating the cerebral effect of ammonia in liver disease.</description><subject>Amino Acids - blood</subject><subject>Amino-acid solution</subject><subject>Aminoacid disorders</subject><subject>Ammonia - blood</subject><subject>Biological and medical sciences</subject><subject>C-Reactive Protein - metabolism</subject><subject>Errors of metabolism</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Hepatic Encephalopathy - complications</subject><subject>Hepatic Encephalopathy - immunology</subject><subject>Hepatic Encephalopathy - psychology</subject><subject>Humans</subject><subject>Hyperammonemia - complications</subject><subject>Hyperammonemia - immunology</subject><subject>Hyperammonemia - psychology</subject><subject>Inflammation - complications</subject><subject>Inflammation - immunology</subject><subject>Inflammation - psychology</subject><subject>Inflammation Mediators - metabolism</subject><subject>Liver Cirrhosis - complications</subject><subject>Liver Cirrhosis - immunology</subject><subject>Liver Cirrhosis - psychology</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mental Recall</subject><subject>Metabolic diseases</subject><subject>Middle Aged</subject><subject>Minimal hepatic encephalopathy</subject><subject>Neuropsychological function</subject><subject>Neuropsychological Tests</subject><subject>Other diseases. Semiology</subject><subject>Proinflammatory cytokines</subject><subject>Reaction Time</subject><issn>0168-8278</issn><issn>1600-0641</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE-L1DAYh4Mo7rj6BTxILu6ts0mbaVPwIsv6BxY8qOeQJm9shrapedtl--19hxnYm7kEfjx5CA9j76XYSyHr2-P-2MO8L4WoaNjT9ILtZC1EIWolX7IdLbrQZaOv2BvEoyBQtOo1u5KqqVrRHnZs_rnhAmN0PE5hsONol5Q3ngHnNCFweLIOcmcXQL70wCdYc5pxc30a0p_o7MAhBHAL8hTI4VcHnvfbDJlkaSK1pZm7mHOfMOJb9irYAeHd5b5mv7_c_7r7Vjz8-Pr97vND4VRbLoWko-pOae1r7-umsar0ylkISluv7KHrah8O2oeqq0IlrQcLQHBnXStEqK7Zzdk75_R3BVzMGNHBMNgJ0opGCymrtm4JLM-gywkxQzBzjqPNm5HCnDqbozl1NqfOp40mevThYl-7Efzzk0tYAj5eAIsUKWQ7uYjP3EFpcjfEfTpzQC0eI2SDLsJEEWOmqsan-L9__ANrjKAq</recordid><startdate>20040201</startdate><enddate>20040201</enddate><creator>Shawcross, Debbie L</creator><creator>Davies, Nathan A</creator><creator>Williams, Roger</creator><creator>Jalan, Rajiv</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</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>20040201</creationdate><title>Systemic inflammatory response exacerbates the neuropsychological effects of induced hyperammonemia in cirrhosis</title><author>Shawcross, Debbie L ; Davies, Nathan A ; Williams, Roger ; Jalan, Rajiv</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c492t-111146b488d6dd677a42d4caef48ad4a5bb6df58df3b3f31adeaee8d6bac900f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Amino Acids - blood</topic><topic>Amino-acid solution</topic><topic>Aminoacid disorders</topic><topic>Ammonia - blood</topic><topic>Biological and medical sciences</topic><topic>C-Reactive Protein - metabolism</topic><topic>Errors of metabolism</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Hepatic Encephalopathy - complications</topic><topic>Hepatic Encephalopathy - immunology</topic><topic>Hepatic Encephalopathy - psychology</topic><topic>Humans</topic><topic>Hyperammonemia - complications</topic><topic>Hyperammonemia - immunology</topic><topic>Hyperammonemia - psychology</topic><topic>Inflammation - complications</topic><topic>Inflammation - immunology</topic><topic>Inflammation - psychology</topic><topic>Inflammation Mediators - metabolism</topic><topic>Liver Cirrhosis - complications</topic><topic>Liver Cirrhosis - immunology</topic><topic>Liver Cirrhosis - psychology</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mental Recall</topic><topic>Metabolic diseases</topic><topic>Middle Aged</topic><topic>Minimal hepatic encephalopathy</topic><topic>Neuropsychological function</topic><topic>Neuropsychological Tests</topic><topic>Other diseases. Semiology</topic><topic>Proinflammatory cytokines</topic><topic>Reaction Time</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shawcross, Debbie L</creatorcontrib><creatorcontrib>Davies, Nathan A</creatorcontrib><creatorcontrib>Williams, Roger</creatorcontrib><creatorcontrib>Jalan, Rajiv</creatorcontrib><collection>Pascal-Francis</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>Journal of hepatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shawcross, Debbie L</au><au>Davies, Nathan A</au><au>Williams, Roger</au><au>Jalan, Rajiv</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Systemic inflammatory response exacerbates the neuropsychological effects of induced hyperammonemia in cirrhosis</atitle><jtitle>Journal of hepatology</jtitle><addtitle>J Hepatol</addtitle><date>2004-02-01</date><risdate>2004</risdate><volume>40</volume><issue>2</issue><spage>247</spage><epage>254</epage><pages>247-254</pages><issn>0168-8278</issn><eissn>1600-0641</eissn><coden>JOHEEC</coden><abstract>Studies in acute liver failure show correlation between evidence of a systemic inflammatory response syndrome (SIRS) and progression of hepatic encephalopathy (HE). We tested the hypothesis that SIRS mediators, such as nitric oxide and proinflammatory cytokines, may exacerbate the neuropsychological effects of hyperammonemia in cirrhosis.
Ten patients with cirrhosis were studied, 24–36 h after admission with clinical evidence of infection, and following its resolution. Hyperammonemia was induced by oral administration of an amino-acid (aa) solution mimicking hemoglobin composition. Inflammatory mediators, nitrate/nitrite, ammonia, aa profiles and a battery of neuropsychological tests were measured.
The hyperammonemia generated in response to the aa solution was similar prior to, and after resolution, of the inflammation (P=0.77). With treatment of the infection there were significant reductions in white blood cell count (WBC), C-reactive protein (CRP), nitrate/nitrite, interleukin-6, interleukin-1β and tumour necrosis factor α. Induced hyperammonemia resulted in significant worsening of the neuropsychological scores when patients showed evidence of SIRS but not after its resolution.
The significant deterioration of neuropsychological test scores following induced hyperammonemia during the inflammatory state, but not after its resolution, suggests that the inflammation and its mediators may be important in modulating the cerebral effect of ammonia in liver disease.</abstract><cop>Oxford</cop><pub>Elsevier B.V</pub><pmid>14739095</pmid><doi>10.1016/j.jhep.2003.10.016</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Amino Acids - blood Amino-acid solution Aminoacid disorders Ammonia - blood Biological and medical sciences C-Reactive Protein - metabolism Errors of metabolism Female Gastroenterology. Liver. Pancreas. Abdomen Hepatic Encephalopathy - complications Hepatic Encephalopathy - immunology Hepatic Encephalopathy - psychology Humans Hyperammonemia - complications Hyperammonemia - immunology Hyperammonemia - psychology Inflammation - complications Inflammation - immunology Inflammation - psychology Inflammation Mediators - metabolism Liver Cirrhosis - complications Liver Cirrhosis - immunology Liver Cirrhosis - psychology Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Mental Recall Metabolic diseases Middle Aged Minimal hepatic encephalopathy Neuropsychological function Neuropsychological Tests Other diseases. Semiology Proinflammatory cytokines Reaction Time |
| title | Systemic inflammatory response exacerbates the neuropsychological effects of induced hyperammonemia in cirrhosis |
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