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Acute liver failure is associated with elevated liver stiffness and hepatic stellate cell activation
Acute liver failure (ALF) is associated with massive short‐term cell death, whereas chronic liver injury is accompanied by continuous cell death. Hepatic stellate cells (HSCs) contribute to tissue repair and liver fibrosis in chronic liver injury, although their role in ALF remains unexplained. Twen...
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| Published in: | Hepatology (Baltimore, Md.) Md.), 2010-09, Vol.52 (3), p.1008-1016 |
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| creator | Dechêne, Alexander Sowa, Jan‐Peter Gieseler, Robert K. Jochum, Christoph Bechmann, Lars P. El Fouly, Amr Schlattjan, Martin Saner, Fuat Baba, Hideo A. Paul, Andreas Dries, Volker Odenthal, Margarethe Gerken, Guido Friedman, Scott L. Canbay, Ali |
| description | Acute liver failure (ALF) is associated with massive short‐term cell death, whereas chronic liver injury is accompanied by continuous cell death. Hepatic stellate cells (HSCs) contribute to tissue repair and liver fibrosis in chronic liver injury, although their role in ALF remains unexplained. Twenty‐nine patients (median age = 43 years, 17 females and 12 males) with ALF according to the Acute Liver Failure Study Group criteria were included. Upon the diagnosis of ALF and after 7 days, we determined liver stiffness (LS) with FibroScan, standard laboratory parameters, and serum levels of matrix metalloproteinase 1 (MMP‐1), MMP‐2, MMP‐9, tissue inhibitor of metalloproteinases 1 (TIMP‐1), TIMP‐2, hyaluronic acid, and markers of overall cell death (M65) and apoptosis (M30). Stellate cell activation and progenitor response were analyzed immunohistochemically in biopsy samples of 12 patients with α‐smooth muscle actin (α‐SMA), keratin‐17, and keratin‐19 staining, respectively. Cell death markers (M30 level = 2243 ± 559.6 U/L, M65 level = 3732 ± 839.9 U/L) and fibrosis markers (TIMP‐1 level = 629.9 ± 69.4 U/mL, MMP‐2 level = 264 ± 32.5 U/mL, hyaluronic acid level = 438.5 ± 69.3 μg/mL) were significantly increased in patients versus healthy controls. This was paralleled by collagen deposition, elevated α‐SMA expression, and higher LS (25.6 ± 3.0 kPa). ALF was associated with ductular progenitor proliferation. Conclusion: Our results demonstrate HSC activation and a progenitor response in ALF. Positive correlations between LS, the degree of liver cell damage, and the intensity of HSC activation suggest that fibrosis is a response to ALF in an attempt to repair damaged tissue. (Hepatology 2010) |
| doi_str_mv | 10.1002/hep.23754 |
| format | article |
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Hepatic stellate cells (HSCs) contribute to tissue repair and liver fibrosis in chronic liver injury, although their role in ALF remains unexplained. Twenty‐nine patients (median age = 43 years, 17 females and 12 males) with ALF according to the Acute Liver Failure Study Group criteria were included. Upon the diagnosis of ALF and after 7 days, we determined liver stiffness (LS) with FibroScan, standard laboratory parameters, and serum levels of matrix metalloproteinase 1 (MMP‐1), MMP‐2, MMP‐9, tissue inhibitor of metalloproteinases 1 (TIMP‐1), TIMP‐2, hyaluronic acid, and markers of overall cell death (M65) and apoptosis (M30). Stellate cell activation and progenitor response were analyzed immunohistochemically in biopsy samples of 12 patients with α‐smooth muscle actin (α‐SMA), keratin‐17, and keratin‐19 staining, respectively. Cell death markers (M30 level = 2243 ± 559.6 U/L, M65 level = 3732 ± 839.9 U/L) and fibrosis markers (TIMP‐1 level = 629.9 ± 69.4 U/mL, MMP‐2 level = 264 ± 32.5 U/mL, hyaluronic acid level = 438.5 ± 69.3 μg/mL) were significantly increased in patients versus healthy controls. This was paralleled by collagen deposition, elevated α‐SMA expression, and higher LS (25.6 ± 3.0 kPa). ALF was associated with ductular progenitor proliferation. Conclusion: Our results demonstrate HSC activation and a progenitor response in ALF. Positive correlations between LS, the degree of liver cell damage, and the intensity of HSC activation suggest that fibrosis is a response to ALF in an attempt to repair damaged tissue. (Hepatology 2010)</description><identifier>ISSN: 0270-9139</identifier><identifier>EISSN: 1527-3350</identifier><identifier>DOI: 10.1002/hep.23754</identifier><identifier>PMID: 20684020</identifier><identifier>CODEN: HPTLD9</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Adult ; Apoptosis ; Biological and medical sciences ; Biomarkers - blood ; Biopsy ; Cell Death ; Elasticity - physiology ; Extracellular Matrix - pathology ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Hepatic Stellate Cells - pathology ; Humans ; Hyaluronic Acid - blood ; Liver - pathology ; Liver Cirrhosis - blood ; Liver Cirrhosis - pathology ; Liver Cirrhosis - physiopathology ; Liver Failure, Acute - blood ; Liver Failure, Acute - pathology ; Liver Failure, Acute - physiopathology ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Matrix Metalloproteinases - blood ; Medical sciences ; Middle Aged ; Other diseases. Semiology ; Retrospective Studies ; Tissue Inhibitor of Metalloproteinase-1 - blood ; Tissue Inhibitor of Metalloproteinase-2 - blood</subject><ispartof>Hepatology (Baltimore, Md.), 2010-09, Vol.52 (3), p.1008-1016</ispartof><rights>Copyright © 2010 American Association for the Study of Liver Diseases</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4504-cfbcb5ef02b758c870de7ce0f9850e786ba261fa66b1c26a789b7d2eb4e84e503</citedby><cites>FETCH-LOGICAL-c4504-cfbcb5ef02b758c870de7ce0f9850e786ba261fa66b1c26a789b7d2eb4e84e503</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fhep.23754$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fhep.23754$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,786,790,27957,27958,50923,51032</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23218623$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20684020$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dechêne, Alexander</creatorcontrib><creatorcontrib>Sowa, Jan‐Peter</creatorcontrib><creatorcontrib>Gieseler, Robert K.</creatorcontrib><creatorcontrib>Jochum, Christoph</creatorcontrib><creatorcontrib>Bechmann, Lars P.</creatorcontrib><creatorcontrib>El Fouly, Amr</creatorcontrib><creatorcontrib>Schlattjan, Martin</creatorcontrib><creatorcontrib>Saner, Fuat</creatorcontrib><creatorcontrib>Baba, Hideo A.</creatorcontrib><creatorcontrib>Paul, Andreas</creatorcontrib><creatorcontrib>Dries, Volker</creatorcontrib><creatorcontrib>Odenthal, Margarethe</creatorcontrib><creatorcontrib>Gerken, Guido</creatorcontrib><creatorcontrib>Friedman, Scott L.</creatorcontrib><creatorcontrib>Canbay, Ali</creatorcontrib><title>Acute liver failure is associated with elevated liver stiffness and hepatic stellate cell activation</title><title>Hepatology (Baltimore, Md.)</title><addtitle>Hepatology</addtitle><description>Acute liver failure (ALF) is associated with massive short‐term cell death, whereas chronic liver injury is accompanied by continuous cell death. Hepatic stellate cells (HSCs) contribute to tissue repair and liver fibrosis in chronic liver injury, although their role in ALF remains unexplained. Twenty‐nine patients (median age = 43 years, 17 females and 12 males) with ALF according to the Acute Liver Failure Study Group criteria were included. Upon the diagnosis of ALF and after 7 days, we determined liver stiffness (LS) with FibroScan, standard laboratory parameters, and serum levels of matrix metalloproteinase 1 (MMP‐1), MMP‐2, MMP‐9, tissue inhibitor of metalloproteinases 1 (TIMP‐1), TIMP‐2, hyaluronic acid, and markers of overall cell death (M65) and apoptosis (M30). Stellate cell activation and progenitor response were analyzed immunohistochemically in biopsy samples of 12 patients with α‐smooth muscle actin (α‐SMA), keratin‐17, and keratin‐19 staining, respectively. Cell death markers (M30 level = 2243 ± 559.6 U/L, M65 level = 3732 ± 839.9 U/L) and fibrosis markers (TIMP‐1 level = 629.9 ± 69.4 U/mL, MMP‐2 level = 264 ± 32.5 U/mL, hyaluronic acid level = 438.5 ± 69.3 μg/mL) were significantly increased in patients versus healthy controls. This was paralleled by collagen deposition, elevated α‐SMA expression, and higher LS (25.6 ± 3.0 kPa). ALF was associated with ductular progenitor proliferation. Conclusion: Our results demonstrate HSC activation and a progenitor response in ALF. Positive correlations between LS, the degree of liver cell damage, and the intensity of HSC activation suggest that fibrosis is a response to ALF in an attempt to repair damaged tissue. (Hepatology 2010)</description><subject>Adult</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - blood</subject><subject>Biopsy</subject><subject>Cell Death</subject><subject>Elasticity - physiology</subject><subject>Extracellular Matrix - pathology</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Hepatic Stellate Cells - pathology</subject><subject>Humans</subject><subject>Hyaluronic Acid - blood</subject><subject>Liver - pathology</subject><subject>Liver Cirrhosis - blood</subject><subject>Liver Cirrhosis - pathology</subject><subject>Liver Cirrhosis - physiopathology</subject><subject>Liver Failure, Acute - blood</subject><subject>Liver Failure, Acute - pathology</subject><subject>Liver Failure, Acute - physiopathology</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Matrix Metalloproteinases - blood</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Other diseases. Semiology</subject><subject>Retrospective Studies</subject><subject>Tissue Inhibitor of Metalloproteinase-1 - blood</subject><subject>Tissue Inhibitor of Metalloproteinase-2 - blood</subject><issn>0270-9139</issn><issn>1527-3350</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNp90c9LHDEUB_BQKnW1PfQfKIEitofRl2TyY44iWguCHux5yGReMDI7syYzK_73Zne2LQh6eiR88r5JHiFfGZwwAH56j6sTLrQsP5AFk1wXQkj4SBbANRQVE9U-OUjpAQCqkptPZJ-DMiVwWJD2zE0j0i6sMVJvQzdFpCFRm9Lggh2xpU9hvKfY4Xq7mmUag_c9pgz7luZ8OwaXd7HrsqIuV2rdGPKZMPSfyZ63XcIvu3pI_lxe3J1fFdc3v36fn10XrpRQFs43rpHogTdaGmc0tKgdgq-MBNRGNZYr5q1SDXNcWW2qRrccmxJNiRLEITme-67i8DhhGutlSJu72B6HKdVaiqrSAmSWP96VTGullOamyvT7K_owTLHP78hKKcOZEWVWP2fl4pBSRF-vYlja-FwzqDdDqvMn1dshZftt13Fqltj-k3-nksHRDtjkbOej7V1I_53ImYqL7E5n9xQ6fH47sb66uJ2jXwAysqiE</recordid><startdate>201009</startdate><enddate>201009</enddate><creator>Dechêne, Alexander</creator><creator>Sowa, Jan‐Peter</creator><creator>Gieseler, Robert K.</creator><creator>Jochum, Christoph</creator><creator>Bechmann, Lars P.</creator><creator>El Fouly, Amr</creator><creator>Schlattjan, Martin</creator><creator>Saner, Fuat</creator><creator>Baba, Hideo A.</creator><creator>Paul, Andreas</creator><creator>Dries, Volker</creator><creator>Odenthal, Margarethe</creator><creator>Gerken, Guido</creator><creator>Friedman, Scott L.</creator><creator>Canbay, Ali</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley</general><general>Wiley Subscription Services, Inc</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>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201009</creationdate><title>Acute liver failure is associated with elevated liver stiffness and hepatic stellate cell activation</title><author>Dechêne, Alexander ; Sowa, Jan‐Peter ; Gieseler, Robert K. ; Jochum, Christoph ; Bechmann, Lars P. ; El Fouly, Amr ; Schlattjan, Martin ; Saner, Fuat ; Baba, Hideo A. ; Paul, Andreas ; Dries, Volker ; Odenthal, Margarethe ; Gerken, Guido ; Friedman, Scott L. ; Canbay, Ali</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4504-cfbcb5ef02b758c870de7ce0f9850e786ba261fa66b1c26a789b7d2eb4e84e503</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adult</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Biomarkers - blood</topic><topic>Biopsy</topic><topic>Cell Death</topic><topic>Elasticity - physiology</topic><topic>Extracellular Matrix - pathology</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Hepatic Stellate Cells - pathology</topic><topic>Humans</topic><topic>Hyaluronic Acid - blood</topic><topic>Liver - pathology</topic><topic>Liver Cirrhosis - blood</topic><topic>Liver Cirrhosis - pathology</topic><topic>Liver Cirrhosis - physiopathology</topic><topic>Liver Failure, Acute - blood</topic><topic>Liver Failure, Acute - pathology</topic><topic>Liver Failure, Acute - physiopathology</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Matrix Metalloproteinases - blood</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Other diseases. 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Hepatic stellate cells (HSCs) contribute to tissue repair and liver fibrosis in chronic liver injury, although their role in ALF remains unexplained. Twenty‐nine patients (median age = 43 years, 17 females and 12 males) with ALF according to the Acute Liver Failure Study Group criteria were included. Upon the diagnosis of ALF and after 7 days, we determined liver stiffness (LS) with FibroScan, standard laboratory parameters, and serum levels of matrix metalloproteinase 1 (MMP‐1), MMP‐2, MMP‐9, tissue inhibitor of metalloproteinases 1 (TIMP‐1), TIMP‐2, hyaluronic acid, and markers of overall cell death (M65) and apoptosis (M30). Stellate cell activation and progenitor response were analyzed immunohistochemically in biopsy samples of 12 patients with α‐smooth muscle actin (α‐SMA), keratin‐17, and keratin‐19 staining, respectively. Cell death markers (M30 level = 2243 ± 559.6 U/L, M65 level = 3732 ± 839.9 U/L) and fibrosis markers (TIMP‐1 level = 629.9 ± 69.4 U/mL, MMP‐2 level = 264 ± 32.5 U/mL, hyaluronic acid level = 438.5 ± 69.3 μg/mL) were significantly increased in patients versus healthy controls. This was paralleled by collagen deposition, elevated α‐SMA expression, and higher LS (25.6 ± 3.0 kPa). ALF was associated with ductular progenitor proliferation. Conclusion: Our results demonstrate HSC activation and a progenitor response in ALF. Positive correlations between LS, the degree of liver cell damage, and the intensity of HSC activation suggest that fibrosis is a response to ALF in an attempt to repair damaged tissue. (Hepatology 2010)</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>20684020</pmid><doi>10.1002/hep.23754</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Apoptosis Biological and medical sciences Biomarkers - blood Biopsy Cell Death Elasticity - physiology Extracellular Matrix - pathology Female Gastroenterology. Liver. Pancreas. Abdomen Hepatic Stellate Cells - pathology Humans Hyaluronic Acid - blood Liver - pathology Liver Cirrhosis - blood Liver Cirrhosis - pathology Liver Cirrhosis - physiopathology Liver Failure, Acute - blood Liver Failure, Acute - pathology Liver Failure, Acute - physiopathology Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Matrix Metalloproteinases - blood Medical sciences Middle Aged Other diseases. Semiology Retrospective Studies Tissue Inhibitor of Metalloproteinase-1 - blood Tissue Inhibitor of Metalloproteinase-2 - blood |
| title | Acute liver failure is associated with elevated liver stiffness and hepatic stellate cell activation |
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