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 Jg. 54; H. 7; S. 987 - 993 |
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| Sprache: | Englisch |
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01.07.2005
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| 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. |
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| AbstractList | 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.
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.
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.
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. 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.AIMSFactors 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.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.METHODSTitres 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.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.RESULTSCirculating 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.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.CONCLUSIONSThese results indicate that the presence of immune reactions triggered by oxidative stress can be an independent predictor of progression of NAFLD 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 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. |
| Author | Saksena, S Day, C P Reale, E Occhino, G Mottaran, E Vidali, M Burt, A D Albano, E |
| AuthorAffiliation | 1 Department of Medical Sciences, University “Amedeo Avogadro” of East Piedmont, Novara, Italy 2 School of Clinical Medical Sciences (Hepatology), Medical School, University of Newcastle, Newcastle upon Tyne, UK |
| AuthorAffiliation_xml | – name: 2 School of Clinical Medical Sciences (Hepatology), Medical School, University of Newcastle, Newcastle upon Tyne, UK – name: 1 Department of Medical Sciences, University “Amedeo Avogadro” of East Piedmont, Novara, Italy |
| Author_xml | – sequence: 1 givenname: E surname: Albano fullname: Albano, E organization: School of Clinical Medical Sciences (Hepatology), Medical School, University of Newcastle, Newcastle upon Tyne, UK – sequence: 2 givenname: E surname: Mottaran fullname: Mottaran, E organization: School of Clinical Medical Sciences (Hepatology), Medical School, University of Newcastle, Newcastle upon Tyne, UK – sequence: 3 givenname: M surname: Vidali fullname: Vidali, M organization: School of Clinical Medical Sciences (Hepatology), Medical School, University of Newcastle, Newcastle upon Tyne, UK – sequence: 4 givenname: E surname: Reale fullname: Reale, E organization: School of Clinical Medical Sciences (Hepatology), Medical School, University of Newcastle, Newcastle upon Tyne, UK – sequence: 5 givenname: S surname: Saksena fullname: Saksena, S organization: School of Clinical Medical Sciences (Hepatology), Medical School, University of Newcastle, Newcastle upon Tyne, UK – sequence: 6 givenname: G surname: Occhino fullname: Occhino, G organization: School of Clinical Medical Sciences (Hepatology), Medical School, University of Newcastle, Newcastle upon Tyne, UK – sequence: 7 givenname: A D surname: Burt fullname: Burt, A D organization: School of Clinical Medical Sciences (Hepatology), Medical School, University of Newcastle, Newcastle upon Tyne, UK – sequence: 8 givenname: C P surname: Day fullname: Day, C P organization: School of Clinical Medical Sciences (Hepatology), Medical School, University of Newcastle, Newcastle upon Tyne, UK |
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| Copyright | Copyright 2005 by Gut 2005 INIST-CNRS Copyright: 2005 Copyright 2005 by Gut Copyright © Copyright 2005 by Gut 2005 |
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| Keywords | Endocrinopathy Type 2 diabetes Obesity Prognosis Immune response Nutrition disorder Hepatic disease Metabolic diseases Lipids Product Arachidonic acid Stress Cirrhosis Non alcoholic steatohepatitis Fibrosis Gastroenterology Digestive diseases Evolution Predictive factor Nutritional status Peroxidation |
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| Notes | href:gutjnl-54-987.pdf ark:/67375/NVC-HDPT3TXT-7 local:0540987 istex:AB9C3243EA8A4CD3480D785FB88B48FCCF8E5906 PMID:15951547 Correspondence to: Professor E Albano Department of Medical Science, University “Amedeo Avogadro” of East Piedmont, Via Solaroli 17, 28100 Novara, Italy; albano@med.unipmn.it ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Conflict of interest: None declared. Correspondence to: Professor E Albano Department of Medical Science, University “Amedeo Avogadro” of East Piedmont, Via Solaroli 17, 28100 Novara, Italy; albano@med.unipmn.it |
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| References_xml | – reference: 11796198 - Free Radic Biol Med. 2002 Jan 15;32(2):110-4 – reference: 10860543 - Arch Biochem Biophys. 2000 Jun 15;378(2):259-68 – reference: 12829994 - Hepatology. 2003 Jul;38(1):123-32 – reference: 14638353 - Am J Gastroenterol. 2003 Nov;98(11):2485-90 – reference: 12668987 - Hepatology. 2003 Apr;37(4):917-23 – reference: 12512031 - Gastroenterology. 2003 Jan;124(1):71-9 – reference: 8907574 - J Hepatol. 1996 Feb;24(2):200-8 – reference: 11097478 - J Hepatol. 2000 Nov;33(5):716-24 – reference: 10839868 - J Pediatr. 2000 Jun;136(6):734-8 – reference: 11483619 - J Lipid Res. 2001 Aug;42(8):1187-96 – reference: 11584369 - Hepatology. 2001 Oct;34(4 Pt 1):729-37 – reference: 12663231 - J Hepatol. 2003 Apr;38(4):414-8 – reference: 15122756 - Hepatology. 2004 May;39(5):1277-85 – reference: 10051466 - Hepatology. 1999 Mar;29(3):664-9 – reference: 11266382 - Gastroenterology. 2001 Apr;120(5):1183-92 – reference: 15307867 - Am J Gastroenterol. 2004 Aug;99(8):1497-502 – reference: 14512879 - Hepatology. 2003 Oct;38(4):919-29 – reference: 2227807 - Hepatology. 1990 Nov;12(5):1106-10 – reference: 10484010 - Am J Gastroenterol. 1999 Sep;94(9):2467-74 – reference: 10772651 - J Clin Invest. 2000 Apr;105(8):1067-75 – reference: 11580156 - J Hepatol. 2001 Aug;35(2):297-306 – reference: 8666344 - Hepatology. 1996 Apr;23(4):872-80 – reference: 7813815 - Diabetes. 1995 Jan;44(1):60-6 – reference: 9547102 - Gastroenterology. 1998 Apr;114(4):842-5 – reference: 9731720 - Pharmacogenetics. 1998 Aug;8(4):335-42 – reference: 12829985 - Hepatology. 2003 Jul;38(1):42-9 – reference: 10733543 - Hepatology. 2000 Apr;31(4):878-84 – reference: 10783322 - Carcinogenesis. 2000 May;21(5):983-9 – reference: 12406438 - Best Pract Res Clin Gastroenterol. 2002 Oct;16(5):663-78 – reference: 8886564 - Diabetes Care. 1996 Oct;19(10):1138-41 – reference: 10963721 - Cardiovasc Res. 2000 Aug 18;47(3):475-88 – reference: 10573511 - Hepatology. 1999 Dec;30(6):1356-62 – reference: 12076862 - J Hepatol. 2002 Jul;37(1):56-62 – reference: 10833486 - Gastroenterology. 2000 Jun;118(6):1117-23 – reference: 15362042 - Gastroenterology. 2004 Sep;127(3):870-82 – reference: 11438497 - Gastroenterology. 2001 Jul;121(1):91-100 – reference: 11709522 - Gut. 2001 Dec;49(6):852-9 – reference: 12668986 - Hepatology. 2003 Apr;37(4):909-16 – reference: 14752838 - Hepatology. 2004 Jan;39(1):197-203 – reference: 15094225 - J Hepatol. 2004 May;40(5):781-6 – reference: 9721166 - Gastroenterology. 1998 Sep;115(3):686-92 – reference: 12830008 - Hepatology. 2003 Jul;38(1):244-51 – reference: 15248380 - Dig Liver Dis. 2004 Jun;36(6):398-405 – reference: 12809815 - Am J Gastroenterol. 2003 May;98(5):960-7 – reference: 14672615 - J Hepatol. 2004 Jan;40(1):60-8 – reference: 11296697 - Semin Liver Dis. 2001;21(1):57-69 – reference: 8550035 - Hepatology. 1996 Jan;23(1):155-63 – reference: 11755315 - Free Radic Biol Med. 2002 Jan 1;32(1):38-45 |
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| Snippet | Aims: Factors responsible for the progression of non-alcoholic fatty liver disease (NAFLD) to more severe liver injury are poorly understood. In the present... Factors responsible for the progression of non-alcoholic fatty liver disease (NAFLD) to more severe liver injury are poorly understood. In the present study,... AIMS: Factors responsible for the progression of non-alcoholic fatty liver disease (NAFLD) to more severe liver injury are poorly understood. In the present... |
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| SubjectTerms | 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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