Characterization and treatment of persistent hepatocellular secretory failure
Background & Aims Hepatocellular secretory failure induced by drugs, toxins or transient biliary obstruction may sometimes persist for months after removal of the initiating factor and may then be fatal without liver transplantation. We characterized patients with severe persistent hepatocellula...
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| Veröffentlicht in: | Liver international 2015-04, Vol.35 (4), p.1478-1488 |
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| creator | van Dijk, Remco Kremer, Andreas E. Smit, Wouter van den Elzen, Bram van Gulik, Thomas Gouma, Dirk Lameris, Johan S. Bikker, Hennie Enemuo, Valentine Stokkers, Pieter C. F. Feist, Mark Bosma, Piter Jansen, Peter L. M. Beuers, Ulrich |
| description | Background & Aims
Hepatocellular secretory failure induced by drugs, toxins or transient biliary obstruction may sometimes persist for months after removal of the initiating factor and may then be fatal without liver transplantation. We characterized patients with severe persistent hepatocellular secretory failure (PHSF) and treated them with the pregnane X receptor (PXR) agonist, rifampicin. We also studied the effect of rifampicin on PXR‐dependent expression of genes involved in biotransformation and secretion in vitro.
Methods
Thirteen patients (age 18–81 years, 6 male) with hepatocellular secretory failure that persisted after removal of the inducing factor (drugs/toxin: 9) or biliary obstruction (4) were identified over 6 years. Six of these patients were screened for ATP8B1 or ABCB11 mutations. All were treated with rifampicin (300 mg daily) for 1–10 weeks. Expression of genes involved in biotransformation and secretion was determined by rtPCR in human hepatocytes and intestinal cells incubated with rifampicin (10 μmol/L).
Results
Serum bilirubin of patients with PHSF ranged from 264 to 755 μmol/L. Normal γGT was found in 10/13 patients of whom 3/6 tested positive for ATP8B1/ABCB11 mutations. Serum bilirubin declined to |
| doi_str_mv | 10.1111/liv.12603 |
| format | Article |
| fullrecord | <record><control><sourceid>istex_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1111_liv_12603</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>ark_67375_WNG_L0LB4BK6_M</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4333-8a02e244cc3ca80eb883600996385b7d11b4a6357ff225f43a90d0d49d11e94a3</originalsourceid><addsrcrecordid>eNp1kE1PwkAQhjdGI4oe_AOmVw-F_erHHoUoEote_DhupttpqBZKdhcVf73FCjfnMjOZZ97DQ8gFowPW1rCuPgaMx1QckBMmkzQUXLDD_cxFj5w690YpUypix6THpaJRwtUJmY3nYMF4tNU3-KpZBrAsAm8R_AKXPmjKYIXWVc5vtzmuwDcG63pdgw0cGou-sZughKpeWzwjRyXUDs__ep883948je_C7HEyHV9noZFCiDAFypFLaYwwkFLM01TElCoVizTKk4KxXEIsoqQsOY9KKUDRghZStRdUEkSfXHW5xjbOWSz1ylYLsBvNqN4q0a0S_aukZS87drXOF1jsyZ2DFhh2wGdV4-b_JJ1NX3aRYfex1fK1_wD7ruNEJJF-fZjojGYjObqP9Uz8ANWSes0</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Characterization and treatment of persistent hepatocellular secretory failure</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>van Dijk, Remco ; Kremer, Andreas E. ; Smit, Wouter ; van den Elzen, Bram ; van Gulik, Thomas ; Gouma, Dirk ; Lameris, Johan S. ; Bikker, Hennie ; Enemuo, Valentine ; Stokkers, Pieter C. F. ; Feist, Mark ; Bosma, Piter ; Jansen, Peter L. M. ; Beuers, Ulrich</creator><creatorcontrib>van Dijk, Remco ; Kremer, Andreas E. ; Smit, Wouter ; van den Elzen, Bram ; van Gulik, Thomas ; Gouma, Dirk ; Lameris, Johan S. ; Bikker, Hennie ; Enemuo, Valentine ; Stokkers, Pieter C. F. ; Feist, Mark ; Bosma, Piter ; Jansen, Peter L. M. ; Beuers, Ulrich</creatorcontrib><description>Background & Aims
Hepatocellular secretory failure induced by drugs, toxins or transient biliary obstruction may sometimes persist for months after removal of the initiating factor and may then be fatal without liver transplantation. We characterized patients with severe persistent hepatocellular secretory failure (PHSF) and treated them with the pregnane X receptor (PXR) agonist, rifampicin. We also studied the effect of rifampicin on PXR‐dependent expression of genes involved in biotransformation and secretion in vitro.
Methods
Thirteen patients (age 18–81 years, 6 male) with hepatocellular secretory failure that persisted after removal of the inducing factor (drugs/toxin: 9) or biliary obstruction (4) were identified over 6 years. Six of these patients were screened for ATP8B1 or ABCB11 mutations. All were treated with rifampicin (300 mg daily) for 1–10 weeks. Expression of genes involved in biotransformation and secretion was determined by rtPCR in human hepatocytes and intestinal cells incubated with rifampicin (10 μmol/L).
Results
Serum bilirubin of patients with PHSF ranged from 264 to 755 μmol/L. Normal γGT was found in 10/13 patients of whom 3/6 tested positive for ATP8B1/ABCB11 mutations. Serum bilirubin declined to <33 μmol/L after 1–10 weeks of rifampicin treatment. In vitro, rifampicin PXR‐dependently upregulated biotransformation phase 1 (CYP3A4), phase 2 (UGT1A1) and phase 3 (MRP2) enzymes/carriers as well as the basolateral bile salt exporter OSTβ.
Conclusion
Persistent hepatocellular secretory failure may develop in carriers of transporter gene mutations. In severe cases, rifampicin may represent an effective therapeutic option of PHSF. PXR‐dependent induction of CYP3A4, UGT1A1, MRP2 and OSTβ could contribute to the anticholestatic effect of rifampicin in PHSF.</description><identifier>ISSN: 1478-3223</identifier><identifier>EISSN: 1478-3231</identifier><identifier>DOI: 10.1111/liv.12603</identifier><identifier>PMID: 24905729</identifier><language>eng</language><publisher>United States: Blackwell Publishing Ltd</publisher><subject>ABCB11 ; Adenosine Triphosphatases - genetics ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; ATP Binding Cassette Transporter, Subfamily B, Member 11 ; ATP-Binding Cassette Transporters - genetics ; ATP8B1 ; Bilirubin - blood ; Chemical and Drug Induced Liver Injury - diagnosis ; Chemical and Drug Induced Liver Injury - drug therapy ; Chemical and Drug Induced Liver Injury - etiology ; Chemical and Drug Induced Liver Injury - physiopathology ; cholestasis ; Cholestasis - complications ; Cholestasis - therapy ; Cytochrome P-450 CYP3A - genetics ; Cytochrome P-450 CYP3A - metabolism ; Cytochrome P-450 CYP3A Inducers - pharmacology ; Female ; Genetic Predisposition to Disease ; Glucuronosyltransferase - genetics ; Glucuronosyltransferase - metabolism ; Hep G2 Cells ; HT29 Cells ; Humans ; Liver - drug effects ; Liver - enzymology ; Liver - metabolism ; Liver Failure - diagnosis ; Liver Failure - drug therapy ; Liver Failure - etiology ; Liver Failure - physiopathology ; Male ; Membrane Transport Proteins - genetics ; Membrane Transport Proteins - metabolism ; Middle Aged ; Multidrug Resistance-Associated Protein 2 ; Multidrug Resistance-Associated Proteins - genetics ; Multidrug Resistance-Associated Proteins - metabolism ; Mutation ; Pregnane X Receptor ; Receptors, Steroid - agonists ; Receptors, Steroid - genetics ; Receptors, Steroid - metabolism ; rifampicin ; Rifampin - therapeutic use ; Risk Factors ; Severity of Illness Index ; Treatment Outcome ; Up-Regulation ; Young Adult</subject><ispartof>Liver international, 2015-04, Vol.35 (4), p.1478-1488</ispartof><rights>2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd</rights><rights>2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4333-8a02e244cc3ca80eb883600996385b7d11b4a6357ff225f43a90d0d49d11e94a3</citedby><cites>FETCH-LOGICAL-c4333-8a02e244cc3ca80eb883600996385b7d11b4a6357ff225f43a90d0d49d11e94a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fliv.12603$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fliv.12603$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24905729$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>van Dijk, Remco</creatorcontrib><creatorcontrib>Kremer, Andreas E.</creatorcontrib><creatorcontrib>Smit, Wouter</creatorcontrib><creatorcontrib>van den Elzen, Bram</creatorcontrib><creatorcontrib>van Gulik, Thomas</creatorcontrib><creatorcontrib>Gouma, Dirk</creatorcontrib><creatorcontrib>Lameris, Johan S.</creatorcontrib><creatorcontrib>Bikker, Hennie</creatorcontrib><creatorcontrib>Enemuo, Valentine</creatorcontrib><creatorcontrib>Stokkers, Pieter C. F.</creatorcontrib><creatorcontrib>Feist, Mark</creatorcontrib><creatorcontrib>Bosma, Piter</creatorcontrib><creatorcontrib>Jansen, Peter L. M.</creatorcontrib><creatorcontrib>Beuers, Ulrich</creatorcontrib><title>Characterization and treatment of persistent hepatocellular secretory failure</title><title>Liver international</title><addtitle>Liver Int</addtitle><description>Background & Aims
Hepatocellular secretory failure induced by drugs, toxins or transient biliary obstruction may sometimes persist for months after removal of the initiating factor and may then be fatal without liver transplantation. We characterized patients with severe persistent hepatocellular secretory failure (PHSF) and treated them with the pregnane X receptor (PXR) agonist, rifampicin. We also studied the effect of rifampicin on PXR‐dependent expression of genes involved in biotransformation and secretion in vitro.
Methods
Thirteen patients (age 18–81 years, 6 male) with hepatocellular secretory failure that persisted after removal of the inducing factor (drugs/toxin: 9) or biliary obstruction (4) were identified over 6 years. Six of these patients were screened for ATP8B1 or ABCB11 mutations. All were treated with rifampicin (300 mg daily) for 1–10 weeks. Expression of genes involved in biotransformation and secretion was determined by rtPCR in human hepatocytes and intestinal cells incubated with rifampicin (10 μmol/L).
Results
Serum bilirubin of patients with PHSF ranged from 264 to 755 μmol/L. Normal γGT was found in 10/13 patients of whom 3/6 tested positive for ATP8B1/ABCB11 mutations. Serum bilirubin declined to <33 μmol/L after 1–10 weeks of rifampicin treatment. In vitro, rifampicin PXR‐dependently upregulated biotransformation phase 1 (CYP3A4), phase 2 (UGT1A1) and phase 3 (MRP2) enzymes/carriers as well as the basolateral bile salt exporter OSTβ.
Conclusion
Persistent hepatocellular secretory failure may develop in carriers of transporter gene mutations. In severe cases, rifampicin may represent an effective therapeutic option of PHSF. PXR‐dependent induction of CYP3A4, UGT1A1, MRP2 and OSTβ could contribute to the anticholestatic effect of rifampicin in PHSF.</description><subject>ABCB11</subject><subject>Adenosine Triphosphatases - genetics</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>ATP Binding Cassette Transporter, Subfamily B, Member 11</subject><subject>ATP-Binding Cassette Transporters - genetics</subject><subject>ATP8B1</subject><subject>Bilirubin - blood</subject><subject>Chemical and Drug Induced Liver Injury - diagnosis</subject><subject>Chemical and Drug Induced Liver Injury - drug therapy</subject><subject>Chemical and Drug Induced Liver Injury - etiology</subject><subject>Chemical and Drug Induced Liver Injury - physiopathology</subject><subject>cholestasis</subject><subject>Cholestasis - complications</subject><subject>Cholestasis - therapy</subject><subject>Cytochrome P-450 CYP3A - genetics</subject><subject>Cytochrome P-450 CYP3A - metabolism</subject><subject>Cytochrome P-450 CYP3A Inducers - pharmacology</subject><subject>Female</subject><subject>Genetic Predisposition to Disease</subject><subject>Glucuronosyltransferase - genetics</subject><subject>Glucuronosyltransferase - metabolism</subject><subject>Hep G2 Cells</subject><subject>HT29 Cells</subject><subject>Humans</subject><subject>Liver - drug effects</subject><subject>Liver - enzymology</subject><subject>Liver - metabolism</subject><subject>Liver Failure - diagnosis</subject><subject>Liver Failure - drug therapy</subject><subject>Liver Failure - etiology</subject><subject>Liver Failure - physiopathology</subject><subject>Male</subject><subject>Membrane Transport Proteins - genetics</subject><subject>Membrane Transport Proteins - metabolism</subject><subject>Middle Aged</subject><subject>Multidrug Resistance-Associated Protein 2</subject><subject>Multidrug Resistance-Associated Proteins - genetics</subject><subject>Multidrug Resistance-Associated Proteins - metabolism</subject><subject>Mutation</subject><subject>Pregnane X Receptor</subject><subject>Receptors, Steroid - agonists</subject><subject>Receptors, Steroid - genetics</subject><subject>Receptors, Steroid - metabolism</subject><subject>rifampicin</subject><subject>Rifampin - therapeutic use</subject><subject>Risk Factors</subject><subject>Severity of Illness Index</subject><subject>Treatment Outcome</subject><subject>Up-Regulation</subject><subject>Young Adult</subject><issn>1478-3223</issn><issn>1478-3231</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kE1PwkAQhjdGI4oe_AOmVw-F_erHHoUoEote_DhupttpqBZKdhcVf73FCjfnMjOZZ97DQ8gFowPW1rCuPgaMx1QckBMmkzQUXLDD_cxFj5w690YpUypix6THpaJRwtUJmY3nYMF4tNU3-KpZBrAsAm8R_AKXPmjKYIXWVc5vtzmuwDcG63pdgw0cGou-sZughKpeWzwjRyXUDs__ep883948je_C7HEyHV9noZFCiDAFypFLaYwwkFLM01TElCoVizTKk4KxXEIsoqQsOY9KKUDRghZStRdUEkSfXHW5xjbOWSz1ylYLsBvNqN4q0a0S_aukZS87drXOF1jsyZ2DFhh2wGdV4-b_JJ1NX3aRYfex1fK1_wD7ruNEJJF-fZjojGYjObqP9Uz8ANWSes0</recordid><startdate>201504</startdate><enddate>201504</enddate><creator>van Dijk, Remco</creator><creator>Kremer, Andreas E.</creator><creator>Smit, Wouter</creator><creator>van den Elzen, Bram</creator><creator>van Gulik, Thomas</creator><creator>Gouma, Dirk</creator><creator>Lameris, Johan S.</creator><creator>Bikker, Hennie</creator><creator>Enemuo, Valentine</creator><creator>Stokkers, Pieter C. F.</creator><creator>Feist, Mark</creator><creator>Bosma, Piter</creator><creator>Jansen, Peter L. M.</creator><creator>Beuers, Ulrich</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</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></search><sort><creationdate>201504</creationdate><title>Characterization and treatment of persistent hepatocellular secretory failure</title><author>van Dijk, Remco ; Kremer, Andreas E. ; Smit, Wouter ; van den Elzen, Bram ; van Gulik, Thomas ; Gouma, Dirk ; Lameris, Johan S. ; Bikker, Hennie ; Enemuo, Valentine ; Stokkers, Pieter C. F. ; Feist, Mark ; Bosma, Piter ; Jansen, Peter L. M. ; Beuers, Ulrich</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4333-8a02e244cc3ca80eb883600996385b7d11b4a6357ff225f43a90d0d49d11e94a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>ABCB11</topic><topic>Adenosine Triphosphatases - genetics</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>ATP Binding Cassette Transporter, Subfamily B, Member 11</topic><topic>ATP-Binding Cassette Transporters - genetics</topic><topic>ATP8B1</topic><topic>Bilirubin - blood</topic><topic>Chemical and Drug Induced Liver Injury - diagnosis</topic><topic>Chemical and Drug Induced Liver Injury - drug therapy</topic><topic>Chemical and Drug Induced Liver Injury - etiology</topic><topic>Chemical and Drug Induced Liver Injury - physiopathology</topic><topic>cholestasis</topic><topic>Cholestasis - complications</topic><topic>Cholestasis - therapy</topic><topic>Cytochrome P-450 CYP3A - genetics</topic><topic>Cytochrome P-450 CYP3A - metabolism</topic><topic>Cytochrome P-450 CYP3A Inducers - pharmacology</topic><topic>Female</topic><topic>Genetic Predisposition to Disease</topic><topic>Glucuronosyltransferase - genetics</topic><topic>Glucuronosyltransferase - metabolism</topic><topic>Hep G2 Cells</topic><topic>HT29 Cells</topic><topic>Humans</topic><topic>Liver - drug effects</topic><topic>Liver - enzymology</topic><topic>Liver - metabolism</topic><topic>Liver Failure - diagnosis</topic><topic>Liver Failure - drug therapy</topic><topic>Liver Failure - etiology</topic><topic>Liver Failure - physiopathology</topic><topic>Male</topic><topic>Membrane Transport Proteins - genetics</topic><topic>Membrane Transport Proteins - metabolism</topic><topic>Middle Aged</topic><topic>Multidrug Resistance-Associated Protein 2</topic><topic>Multidrug Resistance-Associated Proteins - genetics</topic><topic>Multidrug Resistance-Associated Proteins - metabolism</topic><topic>Mutation</topic><topic>Pregnane X Receptor</topic><topic>Receptors, Steroid - agonists</topic><topic>Receptors, Steroid - genetics</topic><topic>Receptors, Steroid - metabolism</topic><topic>rifampicin</topic><topic>Rifampin - therapeutic use</topic><topic>Risk Factors</topic><topic>Severity of Illness Index</topic><topic>Treatment Outcome</topic><topic>Up-Regulation</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>van Dijk, Remco</creatorcontrib><creatorcontrib>Kremer, Andreas E.</creatorcontrib><creatorcontrib>Smit, Wouter</creatorcontrib><creatorcontrib>van den Elzen, Bram</creatorcontrib><creatorcontrib>van Gulik, Thomas</creatorcontrib><creatorcontrib>Gouma, Dirk</creatorcontrib><creatorcontrib>Lameris, Johan S.</creatorcontrib><creatorcontrib>Bikker, Hennie</creatorcontrib><creatorcontrib>Enemuo, Valentine</creatorcontrib><creatorcontrib>Stokkers, Pieter C. F.</creatorcontrib><creatorcontrib>Feist, Mark</creatorcontrib><creatorcontrib>Bosma, Piter</creatorcontrib><creatorcontrib>Jansen, Peter L. M.</creatorcontrib><creatorcontrib>Beuers, Ulrich</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Liver international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>van Dijk, Remco</au><au>Kremer, Andreas E.</au><au>Smit, Wouter</au><au>van den Elzen, Bram</au><au>van Gulik, Thomas</au><au>Gouma, Dirk</au><au>Lameris, Johan S.</au><au>Bikker, Hennie</au><au>Enemuo, Valentine</au><au>Stokkers, Pieter C. F.</au><au>Feist, Mark</au><au>Bosma, Piter</au><au>Jansen, Peter L. M.</au><au>Beuers, Ulrich</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Characterization and treatment of persistent hepatocellular secretory failure</atitle><jtitle>Liver international</jtitle><addtitle>Liver Int</addtitle><date>2015-04</date><risdate>2015</risdate><volume>35</volume><issue>4</issue><spage>1478</spage><epage>1488</epage><pages>1478-1488</pages><issn>1478-3223</issn><eissn>1478-3231</eissn><abstract>Background & Aims
Hepatocellular secretory failure induced by drugs, toxins or transient biliary obstruction may sometimes persist for months after removal of the initiating factor and may then be fatal without liver transplantation. We characterized patients with severe persistent hepatocellular secretory failure (PHSF) and treated them with the pregnane X receptor (PXR) agonist, rifampicin. We also studied the effect of rifampicin on PXR‐dependent expression of genes involved in biotransformation and secretion in vitro.
Methods
Thirteen patients (age 18–81 years, 6 male) with hepatocellular secretory failure that persisted after removal of the inducing factor (drugs/toxin: 9) or biliary obstruction (4) were identified over 6 years. Six of these patients were screened for ATP8B1 or ABCB11 mutations. All were treated with rifampicin (300 mg daily) for 1–10 weeks. Expression of genes involved in biotransformation and secretion was determined by rtPCR in human hepatocytes and intestinal cells incubated with rifampicin (10 μmol/L).
Results
Serum bilirubin of patients with PHSF ranged from 264 to 755 μmol/L. Normal γGT was found in 10/13 patients of whom 3/6 tested positive for ATP8B1/ABCB11 mutations. Serum bilirubin declined to <33 μmol/L after 1–10 weeks of rifampicin treatment. In vitro, rifampicin PXR‐dependently upregulated biotransformation phase 1 (CYP3A4), phase 2 (UGT1A1) and phase 3 (MRP2) enzymes/carriers as well as the basolateral bile salt exporter OSTβ.
Conclusion
Persistent hepatocellular secretory failure may develop in carriers of transporter gene mutations. In severe cases, rifampicin may represent an effective therapeutic option of PHSF. PXR‐dependent induction of CYP3A4, UGT1A1, MRP2 and OSTβ could contribute to the anticholestatic effect of rifampicin in PHSF.</abstract><cop>United States</cop><pub>Blackwell Publishing Ltd</pub><pmid>24905729</pmid><doi>10.1111/liv.12603</doi><tpages>11</tpages></addata></record> |
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| ispartof | Liver international, 2015-04, Vol.35 (4), p.1478-1488 |
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| subjects | ABCB11 Adenosine Triphosphatases - genetics Adolescent Adult Aged Aged, 80 and over ATP Binding Cassette Transporter, Subfamily B, Member 11 ATP-Binding Cassette Transporters - genetics ATP8B1 Bilirubin - blood Chemical and Drug Induced Liver Injury - diagnosis Chemical and Drug Induced Liver Injury - drug therapy Chemical and Drug Induced Liver Injury - etiology Chemical and Drug Induced Liver Injury - physiopathology cholestasis Cholestasis - complications Cholestasis - therapy Cytochrome P-450 CYP3A - genetics Cytochrome P-450 CYP3A - metabolism Cytochrome P-450 CYP3A Inducers - pharmacology Female Genetic Predisposition to Disease Glucuronosyltransferase - genetics Glucuronosyltransferase - metabolism Hep G2 Cells HT29 Cells Humans Liver - drug effects Liver - enzymology Liver - metabolism Liver Failure - diagnosis Liver Failure - drug therapy Liver Failure - etiology Liver Failure - physiopathology Male Membrane Transport Proteins - genetics Membrane Transport Proteins - metabolism Middle Aged Multidrug Resistance-Associated Protein 2 Multidrug Resistance-Associated Proteins - genetics Multidrug Resistance-Associated Proteins - metabolism Mutation Pregnane X Receptor Receptors, Steroid - agonists Receptors, Steroid - genetics Receptors, Steroid - metabolism rifampicin Rifampin - therapeutic use Risk Factors Severity of Illness Index Treatment Outcome Up-Regulation Young Adult |
| title | Characterization and treatment of persistent hepatocellular secretory failure |
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