Immune response towards lipid peroxidation products as a predictor of progression of non-alcoholic fatty liver disease to advanced fibrosis
Aims: Factors responsible for the progression of non-alcoholic fatty liver disease (NAFLD) to more severe liver injury are poorly understood. In the present study, we investigated the association between immune reactions triggered by oxidative stress and stage of NAFLD. Methods: Titres of IgG agains...
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| Veröffentlicht in: | Gut 2005-07, Vol.54 (7), p.987-993 |
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| creator | Albano, E Mottaran, E Vidali, M Reale, E Saksena, S Occhino, G Burt, A D Day, C P |
| description | Aims: Factors responsible for the progression of non-alcoholic fatty liver disease (NAFLD) to more severe liver injury are poorly understood. In the present study, we investigated the association between immune reactions triggered by oxidative stress and stage of NAFLD. Methods: Titres of IgG against human serum albumin adducted with malondialdehyde (MDA-HSA) or arachidonic acid hydroperoxide (AAHP) and against oxidised cardiolipin (Ox-CL) were measured in 167 NAFLD patients with steatosis only (n = 79), steatohepatitis (n = 74), or steatosis plus cirrhosis (n = 14), and in 59 age and sex matched controls. Results: Circulating IgG against lipid peroxidation products was significantly higher (p |
| doi_str_mv | 10.1136/gut.2004.057968 |
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| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1774606</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>67924695</sourcerecordid><originalsourceid>FETCH-LOGICAL-b619t-8c915495c2af192b9ab28f602385254b33d1f5b19e188fdd06b573050d656c033</originalsourceid><addsrcrecordid>eNqFkk1rFDEYxwdR7Fo9e5OA6EGYbV4mbxdBVm0LRT2s4i1kksw268xkTGbW9jP4pZtxl1a9FALh4fnl_7zkXxTPEVwiRNjJZhqXGMJqCSmXTDwoFqhioiRYiIfFAkLES8oreVQ8SWkLIRRCosfFEaKSIlrxRfH7vOum3oHo0hD65MAYfuloE2j94C0YXAxX3urRhx4MMdjJjAnofHLkrDdjiCA0c2qTJdKM5bAPfalbEy5D6w1o9DheZ8Gdi8D65PSfMkDbne6Ns6DxdQzJp6fFo0a3yT073MfF148f1quz8uLz6fnq3UVZMyTHUhiZe5fUYN0giWupaywaBjERFNOqJsSihtZIOiREYy1kNeUEUmgZZQYScly83esOU905a1w_Rt2qIfpOx2sVtFf_Znp_qTZhpxDnFYMsC7w-CMTwc3JpVJ1PxrWt7l2YkmJc4opJei-IIZcciRl8-R-4DVPs8xbmopIQiHmVqZM9ZfK-UnTNbc8IqtkPKvtBzX5Qez_kFy_-HvWOPxggA68OgE5Gt03MX-LTHceEJJXEmSv3nE-ju7rN6_gjT0s4VZ--rdTZ-y9rsv6-VrPumz1fd9t7u7wBYGvdgA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1779330274</pqid></control><display><type>article</type><title>Immune response towards lipid peroxidation products as a predictor of progression of non-alcoholic fatty liver disease to advanced fibrosis</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Albano, E ; Mottaran, E ; Vidali, M ; Reale, E ; Saksena, S ; Occhino, G ; Burt, A D ; Day, C P</creator><creatorcontrib>Albano, E ; Mottaran, E ; Vidali, M ; Reale, E ; Saksena, S ; Occhino, G ; Burt, A D ; Day, C P</creatorcontrib><description>Aims: Factors responsible for the progression of non-alcoholic fatty liver disease (NAFLD) to more severe liver injury are poorly understood. In the present study, we investigated the association between immune reactions triggered by oxidative stress and stage of NAFLD. Methods: Titres of IgG against human serum albumin adducted with malondialdehyde (MDA-HSA) or arachidonic acid hydroperoxide (AAHP) and against oxidised cardiolipin (Ox-CL) were measured in 167 NAFLD patients with steatosis only (n = 79), steatohepatitis (n = 74), or steatosis plus cirrhosis (n = 14), and in 59 age and sex matched controls. Results: Circulating IgG against lipid peroxidation products was significantly higher (p<0.001) in NAFLD patients than in controls. Oxidative stress dependent immune responses were not associated with obesity, type 2 diabetes, or with serum cholesterol, ferritin, or aminotransferase levels. Titres of lipid peroxidation related antibodies were also independent of the extent of steatosis and were similarly distributed in patients with and without necroinflammation. In contrast, the same antibodies were significantly increased in patients with advanced fibrosis or cirrhosis. Logistic regression analysis confirmed that anti-MDA antibodies were independently associated with progression of NALFD and that NAFLD patients with titres of anti-MDA-HSA antibodies above the control threshold value had a threefold (relative risk 2.82 (95% confidence interval 1.35–5.90); p = 0.007) higher risk of having advanced fibrosis/cirrhosis than patients whose antibody titres were within the control range. Conclusions: These results indicate that the presence of immune reactions triggered by oxidative stress can be an independent predictor of progression of NAFLD to advanced fibrosis.</description><identifier>ISSN: 0017-5749</identifier><identifier>EISSN: 1468-3288</identifier><identifier>EISSN: 1458-3288</identifier><identifier>DOI: 10.1136/gut.2004.057968</identifier><identifier>PMID: 15951547</identifier><identifier>CODEN: GUTTAK</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and British Society of Gastroenterology</publisher><subject>4-dihydropyridine-3 ; 4-HNE ; 4-hydroxynonenal ; 4-methyl-1 ; 5-dicarbaldehyde ; AAHP-HSA ; Adult ; Aged ; arachidonic acid hydroperoxide adduct with human serum albumin ; aspartate aminotransferase/alanine aminotransferase ; AST/ALT ; Autoantibodies - blood ; Biological and medical sciences ; Biomarkers - blood ; BMI ; body mass index ; Diabetes. Impaired glucose tolerance ; Disease Progression ; ELISA ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; enzyme linked immunoabsorbent assay ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Fatty Liver - complications ; Fatty Liver - immunology ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; HSA ; HSC ; human hepatic stellate cells ; human serum albumin ; Humans ; immune mechanisms ; Immunoglobulin G - blood ; Laboratories ; Lipid Peroxidation - immunology ; Liver cirrhosis ; Liver Cirrhosis - etiology ; Liver Cirrhosis - immunology ; Liver Disease ; liver fibrosis ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Logistic Models ; Male ; Malondialdehyde - immunology ; malondialdehyde adduct with human serum albumin ; MDA-HSA ; MDD ; Medical sciences ; Metabolic diseases ; Middle Aged ; NAFLD ; NASH ; non-alcoholic fatty liver disease ; non-alcoholic steatohepatitis ; Obesity ; Other diseases. Semiology ; Ox-CL ; oxidative stress ; Oxidative Stress - immunology ; oxidised cardiolipin ; PBS ; phosphate buffered saline ; Rodents ; Serum Albumin - immunology ; steatosis ; Studies ; Womens health</subject><ispartof>Gut, 2005-07, Vol.54 (7), p.987-993</ispartof><rights>Copyright 2005 by Gut</rights><rights>2005 INIST-CNRS</rights><rights>Copyright: 2005 Copyright 2005 by Gut</rights><rights>Copyright © Copyright 2005 by Gut 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b619t-8c915495c2af192b9ab28f602385254b33d1f5b19e188fdd06b573050d656c033</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1774606/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1774606/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16893492$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15951547$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Albano, E</creatorcontrib><creatorcontrib>Mottaran, E</creatorcontrib><creatorcontrib>Vidali, M</creatorcontrib><creatorcontrib>Reale, E</creatorcontrib><creatorcontrib>Saksena, S</creatorcontrib><creatorcontrib>Occhino, G</creatorcontrib><creatorcontrib>Burt, A D</creatorcontrib><creatorcontrib>Day, C P</creatorcontrib><title>Immune response towards lipid peroxidation products as a predictor of progression of non-alcoholic fatty liver disease to advanced fibrosis</title><title>Gut</title><addtitle>Gut</addtitle><description>Aims: Factors responsible for the progression of non-alcoholic fatty liver disease (NAFLD) to more severe liver injury are poorly understood. In the present study, we investigated the association between immune reactions triggered by oxidative stress and stage of NAFLD. Methods: Titres of IgG against human serum albumin adducted with malondialdehyde (MDA-HSA) or arachidonic acid hydroperoxide (AAHP) and against oxidised cardiolipin (Ox-CL) were measured in 167 NAFLD patients with steatosis only (n = 79), steatohepatitis (n = 74), or steatosis plus cirrhosis (n = 14), and in 59 age and sex matched controls. Results: Circulating IgG against lipid peroxidation products was significantly higher (p<0.001) in NAFLD patients than in controls. Oxidative stress dependent immune responses were not associated with obesity, type 2 diabetes, or with serum cholesterol, ferritin, or aminotransferase levels. Titres of lipid peroxidation related antibodies were also independent of the extent of steatosis and were similarly distributed in patients with and without necroinflammation. In contrast, the same antibodies were significantly increased in patients with advanced fibrosis or cirrhosis. Logistic regression analysis confirmed that anti-MDA antibodies were independently associated with progression of NALFD and that NAFLD patients with titres of anti-MDA-HSA antibodies above the control threshold value had a threefold (relative risk 2.82 (95% confidence interval 1.35–5.90); p = 0.007) higher risk of having advanced fibrosis/cirrhosis than patients whose antibody titres were within the control range. Conclusions: These results indicate that the presence of immune reactions triggered by oxidative stress can be an independent predictor of progression of NAFLD to advanced fibrosis.</description><subject>4-dihydropyridine-3</subject><subject>4-HNE</subject><subject>4-hydroxynonenal</subject><subject>4-methyl-1</subject><subject>5-dicarbaldehyde</subject><subject>AAHP-HSA</subject><subject>Adult</subject><subject>Aged</subject><subject>arachidonic acid hydroperoxide adduct with human serum albumin</subject><subject>aspartate aminotransferase/alanine aminotransferase</subject><subject>AST/ALT</subject><subject>Autoantibodies - blood</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - blood</subject><subject>BMI</subject><subject>body mass index</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Disease Progression</subject><subject>ELISA</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>enzyme linked immunoabsorbent assay</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Fatty Liver - complications</subject><subject>Fatty Liver - immunology</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>HSA</subject><subject>HSC</subject><subject>human hepatic stellate cells</subject><subject>human serum albumin</subject><subject>Humans</subject><subject>immune mechanisms</subject><subject>Immunoglobulin G - blood</subject><subject>Laboratories</subject><subject>Lipid Peroxidation - immunology</subject><subject>Liver cirrhosis</subject><subject>Liver Cirrhosis - etiology</subject><subject>Liver Cirrhosis - immunology</subject><subject>Liver Disease</subject><subject>liver fibrosis</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Logistic Models</subject><subject>Male</subject><subject>Malondialdehyde - immunology</subject><subject>malondialdehyde adduct with human serum albumin</subject><subject>MDA-HSA</subject><subject>MDD</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Middle Aged</subject><subject>NAFLD</subject><subject>NASH</subject><subject>non-alcoholic fatty liver disease</subject><subject>non-alcoholic steatohepatitis</subject><subject>Obesity</subject><subject>Other diseases. Semiology</subject><subject>Ox-CL</subject><subject>oxidative stress</subject><subject>Oxidative Stress - immunology</subject><subject>oxidised cardiolipin</subject><subject>PBS</subject><subject>phosphate buffered saline</subject><subject>Rodents</subject><subject>Serum Albumin - immunology</subject><subject>steatosis</subject><subject>Studies</subject><subject>Womens health</subject><issn>0017-5749</issn><issn>1468-3288</issn><issn>1458-3288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkk1rFDEYxwdR7Fo9e5OA6EGYbV4mbxdBVm0LRT2s4i1kksw268xkTGbW9jP4pZtxl1a9FALh4fnl_7zkXxTPEVwiRNjJZhqXGMJqCSmXTDwoFqhioiRYiIfFAkLES8oreVQ8SWkLIRRCosfFEaKSIlrxRfH7vOum3oHo0hD65MAYfuloE2j94C0YXAxX3urRhx4MMdjJjAnofHLkrDdjiCA0c2qTJdKM5bAPfalbEy5D6w1o9DheZ8Gdi8D65PSfMkDbne6Ns6DxdQzJp6fFo0a3yT073MfF148f1quz8uLz6fnq3UVZMyTHUhiZe5fUYN0giWupaywaBjERFNOqJsSihtZIOiREYy1kNeUEUmgZZQYScly83esOU905a1w_Rt2qIfpOx2sVtFf_Znp_qTZhpxDnFYMsC7w-CMTwc3JpVJ1PxrWt7l2YkmJc4opJei-IIZcciRl8-R-4DVPs8xbmopIQiHmVqZM9ZfK-UnTNbc8IqtkPKvtBzX5Qez_kFy_-HvWOPxggA68OgE5Gt03MX-LTHceEJJXEmSv3nE-ju7rN6_gjT0s4VZ--rdTZ-y9rsv6-VrPumz1fd9t7u7wBYGvdgA</recordid><startdate>20050701</startdate><enddate>20050701</enddate><creator>Albano, E</creator><creator>Mottaran, E</creator><creator>Vidali, M</creator><creator>Reale, E</creator><creator>Saksena, S</creator><creator>Occhino, G</creator><creator>Burt, A D</creator><creator>Day, C P</creator><general>BMJ Publishing Group Ltd and British Society of Gastroenterology</general><general>BMJ</general><general>BMJ Publishing Group LTD</general><general>Copyright 2005 by Gut</general><scope>BSCLL</scope><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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20050701</creationdate><title>Immune response towards lipid peroxidation products as a predictor of progression of non-alcoholic fatty liver disease to advanced fibrosis</title><author>Albano, E ; Mottaran, E ; Vidali, M ; Reale, E ; Saksena, S ; Occhino, G ; Burt, A D ; Day, C P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b619t-8c915495c2af192b9ab28f602385254b33d1f5b19e188fdd06b573050d656c033</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>4-dihydropyridine-3</topic><topic>4-HNE</topic><topic>4-hydroxynonenal</topic><topic>4-methyl-1</topic><topic>5-dicarbaldehyde</topic><topic>AAHP-HSA</topic><topic>Adult</topic><topic>Aged</topic><topic>arachidonic acid hydroperoxide adduct with human serum albumin</topic><topic>aspartate aminotransferase/alanine aminotransferase</topic><topic>AST/ALT</topic><topic>Autoantibodies - blood</topic><topic>Biological and medical sciences</topic><topic>Biomarkers - blood</topic><topic>BMI</topic><topic>body mass index</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Disease Progression</topic><topic>ELISA</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>enzyme linked immunoabsorbent assay</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Fatty Liver - complications</topic><topic>Fatty Liver - immunology</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>HSA</topic><topic>HSC</topic><topic>human hepatic stellate cells</topic><topic>human serum albumin</topic><topic>Humans</topic><topic>immune mechanisms</topic><topic>Immunoglobulin G - blood</topic><topic>Laboratories</topic><topic>Lipid Peroxidation - immunology</topic><topic>Liver cirrhosis</topic><topic>Liver Cirrhosis - etiology</topic><topic>Liver Cirrhosis - immunology</topic><topic>Liver Disease</topic><topic>liver fibrosis</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Logistic Models</topic><topic>Male</topic><topic>Malondialdehyde - immunology</topic><topic>malondialdehyde adduct with human serum albumin</topic><topic>MDA-HSA</topic><topic>MDD</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Middle Aged</topic><topic>NAFLD</topic><topic>NASH</topic><topic>non-alcoholic fatty liver disease</topic><topic>non-alcoholic steatohepatitis</topic><topic>Obesity</topic><topic>Other diseases. Semiology</topic><topic>Ox-CL</topic><topic>oxidative stress</topic><topic>Oxidative Stress - immunology</topic><topic>oxidised cardiolipin</topic><topic>PBS</topic><topic>phosphate buffered saline</topic><topic>Rodents</topic><topic>Serum Albumin - immunology</topic><topic>steatosis</topic><topic>Studies</topic><topic>Womens health</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Albano, E</creatorcontrib><creatorcontrib>Mottaran, E</creatorcontrib><creatorcontrib>Vidali, M</creatorcontrib><creatorcontrib>Reale, E</creatorcontrib><creatorcontrib>Saksena, S</creatorcontrib><creatorcontrib>Occhino, G</creatorcontrib><creatorcontrib>Burt, A D</creatorcontrib><creatorcontrib>Day, C P</creatorcontrib><collection>Istex</collection><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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Gut</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Albano, E</au><au>Mottaran, E</au><au>Vidali, M</au><au>Reale, E</au><au>Saksena, S</au><au>Occhino, G</au><au>Burt, A D</au><au>Day, C P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Immune response towards lipid peroxidation products as a predictor of progression of non-alcoholic fatty liver disease to advanced fibrosis</atitle><jtitle>Gut</jtitle><addtitle>Gut</addtitle><date>2005-07-01</date><risdate>2005</risdate><volume>54</volume><issue>7</issue><spage>987</spage><epage>993</epage><pages>987-993</pages><issn>0017-5749</issn><eissn>1468-3288</eissn><eissn>1458-3288</eissn><coden>GUTTAK</coden><abstract>Aims: Factors responsible for the progression of non-alcoholic fatty liver disease (NAFLD) to more severe liver injury are poorly understood. In the present study, we investigated the association between immune reactions triggered by oxidative stress and stage of NAFLD. Methods: Titres of IgG against human serum albumin adducted with malondialdehyde (MDA-HSA) or arachidonic acid hydroperoxide (AAHP) and against oxidised cardiolipin (Ox-CL) were measured in 167 NAFLD patients with steatosis only (n = 79), steatohepatitis (n = 74), or steatosis plus cirrhosis (n = 14), and in 59 age and sex matched controls. Results: Circulating IgG against lipid peroxidation products was significantly higher (p<0.001) in NAFLD patients than in controls. Oxidative stress dependent immune responses were not associated with obesity, type 2 diabetes, or with serum cholesterol, ferritin, or aminotransferase levels. Titres of lipid peroxidation related antibodies were also independent of the extent of steatosis and were similarly distributed in patients with and without necroinflammation. In contrast, the same antibodies were significantly increased in patients with advanced fibrosis or cirrhosis. Logistic regression analysis confirmed that anti-MDA antibodies were independently associated with progression of NALFD and that NAFLD patients with titres of anti-MDA-HSA antibodies above the control threshold value had a threefold (relative risk 2.82 (95% confidence interval 1.35–5.90); p = 0.007) higher risk of having advanced fibrosis/cirrhosis than patients whose antibody titres were within the control range. Conclusions: These results indicate that the presence of immune reactions triggered by oxidative stress can be an independent predictor of progression of NAFLD to advanced fibrosis.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and British Society of Gastroenterology</pub><pmid>15951547</pmid><doi>10.1136/gut.2004.057968</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Gut, 2005-07, Vol.54 (7), p.987-993 |
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| language | eng |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection |
| subjects | 4-dihydropyridine-3 4-HNE 4-hydroxynonenal 4-methyl-1 5-dicarbaldehyde AAHP-HSA Adult Aged arachidonic acid hydroperoxide adduct with human serum albumin aspartate aminotransferase/alanine aminotransferase AST/ALT Autoantibodies - blood Biological and medical sciences Biomarkers - blood BMI body mass index Diabetes. Impaired glucose tolerance Disease Progression ELISA Endocrine pancreas. Apud cells (diseases) Endocrinopathies enzyme linked immunoabsorbent assay Etiopathogenesis. Screening. Investigations. Target tissue resistance Fatty Liver - complications Fatty Liver - immunology Female Gastroenterology. Liver. Pancreas. Abdomen HSA HSC human hepatic stellate cells human serum albumin Humans immune mechanisms Immunoglobulin G - blood Laboratories Lipid Peroxidation - immunology Liver cirrhosis Liver Cirrhosis - etiology Liver Cirrhosis - immunology Liver Disease liver fibrosis Liver. Biliary tract. Portal circulation. Exocrine pancreas Logistic Models Male Malondialdehyde - immunology malondialdehyde adduct with human serum albumin MDA-HSA MDD Medical sciences Metabolic diseases Middle Aged NAFLD NASH non-alcoholic fatty liver disease non-alcoholic steatohepatitis Obesity Other diseases. Semiology Ox-CL oxidative stress Oxidative Stress - immunology oxidised cardiolipin PBS phosphate buffered saline Rodents Serum Albumin - immunology steatosis Studies Womens health |
| title | Immune response towards lipid peroxidation products as a predictor of progression of non-alcoholic fatty liver disease to advanced fibrosis |
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