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Dynamics of liver stiffness by transient elastography in patients with chronic hepatitis C virus infection receiving direct‐acting antiviral therapy—Results from the German Hepatitis C‐Registry
The impact of direct‐acting antiviral (DAA) therapies on fibrosis regression remains uncertain. In the current study, we prospectively evaluated dynamics of liver stiffness by transient elastography (TE) in patients with chronic HCV infection receiving DAA‐based treatment. Patients (260) were enroll...
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Published in: | Journal of viral hepatitis 2020-07, Vol.27 (7), p.690-698 |
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container_title | Journal of viral hepatitis |
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creator | Knop, Viola Mauss, Stefan Goeser, Tobias Geier, Andreas Zimmermann, Tim Herzer, Kerstin Postel, Nils Friedrich‐Rust, Mireen Hofmann, Wolf Peter Ende, Katrin Pathil, Anita Bauer, Tilman Zeuzem, Stefan Berg, Thomas Cornberg, Markus Börner, Norbert Ringelhan, Marc Klinker, Hartwig Schlenker, Thorsten Lutz, Thomas Heinzow, Hauke Günther, Rainer Busch, Heiner Baumgarten, Axel Buggisch, Peter Roessle, Martin Hüppe, Dietrich Manns, Michael P. Niederau, Claus Sarrazin, Christoph Schirmacher, Peter Simon, Karl‐Georg Wedemeyer, Heiner |
description | The impact of direct‐acting antiviral (DAA) therapies on fibrosis regression remains uncertain. In the current study, we prospectively evaluated dynamics of liver stiffness by transient elastography (TE) in patients with chronic HCV infection receiving DAA‐based treatment. Patients (260) were enrolled in the German Hepatitis C‐Registry (DHC‐R), a national multicentre real‐world cohort. Liver stiffness (LS) was assessed at baseline, end of treatment (EOT) and 24 weeks after EOT (FU24) by TE. Biochemical, virological and clinical data were obtained in parallel. In patients with SVR, there was a significant improvement of LS between baseline (median [range], 8.6 [1.7‐73.5] kPa) and FU24 (7.9 [1.7‐75 kPa]; P |
doi_str_mv | 10.1111/jvh.13280 |
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In the current study, we prospectively evaluated dynamics of liver stiffness by transient elastography (TE) in patients with chronic HCV infection receiving DAA‐based treatment. Patients (260) were enrolled in the German Hepatitis C‐Registry (DHC‐R), a national multicentre real‐world cohort. Liver stiffness (LS) was assessed at baseline, end of treatment (EOT) and 24 weeks after EOT (FU24) by TE. Biochemical, virological and clinical data were obtained in parallel. In patients with SVR, there was a significant improvement of LS between baseline (median [range], 8.6 [1.7‐73.5] kPa) and FU24 (7.9 [1.7‐75 kPa]; P < .0001) as well as between EOT (8.4 [1.7‐73.5 kPa]) and FU24 [P < .0001]. Stratified by fibrosis stage, patients classified into F4 had higher magnitude of LS reduction between BL (median [range], 25.1 [13.5‐73.5] kPa) and FU24 (21.5 [3.1‐75] kPa; P = .002) compared to those with F2‐F3 (8.9 [7.1‐12.4] kPa and 8.8 [4.2‐29.1]; P = .060) or F0‐F1 (5.3 [1.7‐7] kPa and 5.2 [1.7‐7.7]; P = .064). In cirrhotic patients, low platelets were significantly associated with lack of liver stiffness improvement, both at EOT (P = .018) and at FU24 (P = .012). LS significantly correlated with ALT (r = .371), AST (r = .552), platelets (r = −.499), GGT (r = .250), bilirubin (r = .230), APRI score (r = .512), FIB‐4 score (r = .517) and FORNS index (r = .562); P < .0001. Liver elastography improved significantly in our real‐world cohort after DAA‐based therapy. As LS correlates similarly with transaminase levels and serum fibrosis markers, it might reflect both reduction of necroinflammation and fibrosis regression.</description><identifier>ISSN: 1352-0504</identifier><identifier>EISSN: 1365-2893</identifier><identifier>DOI: 10.1111/jvh.13280</identifier><identifier>PMID: 32096310</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Antiviral agents ; Antiviral drugs ; Bilirubin ; chronic hepatitis C ; Chronic infection ; direct‐acting antiviral (DAA) treatment ; Fibrosis ; Hepatitis C ; Interferon ; Liver ; Patients ; Platelets ; Transaminase ; transient elastography</subject><ispartof>Journal of viral hepatitis, 2020-07, Vol.27 (7), p.690-698</ispartof><rights>2020 John Wiley & Sons Ltd</rights><rights>2020 John Wiley & Sons Ltd.</rights><rights>Copyright © 2020 John Wiley & Sons Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3530-bead6ac294a6eddef855dd87df730a51be2080294d87bedc9bb4329f051c775e3</citedby><cites>FETCH-LOGICAL-c3530-bead6ac294a6eddef855dd87df730a51be2080294d87bedc9bb4329f051c775e3</cites><orcidid>0000-0002-7434-5218</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32096310$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Knop, Viola</creatorcontrib><creatorcontrib>Mauss, Stefan</creatorcontrib><creatorcontrib>Goeser, Tobias</creatorcontrib><creatorcontrib>Geier, Andreas</creatorcontrib><creatorcontrib>Zimmermann, Tim</creatorcontrib><creatorcontrib>Herzer, Kerstin</creatorcontrib><creatorcontrib>Postel, Nils</creatorcontrib><creatorcontrib>Friedrich‐Rust, Mireen</creatorcontrib><creatorcontrib>Hofmann, Wolf Peter</creatorcontrib><creatorcontrib>Ende, Katrin</creatorcontrib><creatorcontrib>Pathil, Anita</creatorcontrib><creatorcontrib>Bauer, Tilman</creatorcontrib><creatorcontrib>Zeuzem, Stefan</creatorcontrib><creatorcontrib>Berg, Thomas</creatorcontrib><creatorcontrib>Cornberg, Markus</creatorcontrib><creatorcontrib>Börner, Norbert</creatorcontrib><creatorcontrib>Ringelhan, Marc</creatorcontrib><creatorcontrib>Klinker, Hartwig</creatorcontrib><creatorcontrib>Schlenker, Thorsten</creatorcontrib><creatorcontrib>Lutz, Thomas</creatorcontrib><creatorcontrib>Heinzow, Hauke</creatorcontrib><creatorcontrib>Günther, Rainer</creatorcontrib><creatorcontrib>Busch, Heiner</creatorcontrib><creatorcontrib>Baumgarten, Axel</creatorcontrib><creatorcontrib>Buggisch, Peter</creatorcontrib><creatorcontrib>Roessle, Martin</creatorcontrib><creatorcontrib>Hüppe, Dietrich</creatorcontrib><creatorcontrib>Manns, Michael P.</creatorcontrib><creatorcontrib>Niederau, Claus</creatorcontrib><creatorcontrib>Sarrazin, Christoph</creatorcontrib><creatorcontrib>Schirmacher, Peter</creatorcontrib><creatorcontrib>Simon, Karl‐Georg</creatorcontrib><creatorcontrib>Wedemeyer, Heiner</creatorcontrib><creatorcontrib>German Hepatitis C-Registry</creatorcontrib><creatorcontrib>German Hepatitis C‐Registry</creatorcontrib><title>Dynamics of liver stiffness by transient elastography in patients with chronic hepatitis C virus infection receiving direct‐acting antiviral therapy—Results from the German Hepatitis C‐Registry</title><title>Journal of viral hepatitis</title><addtitle>J Viral Hepat</addtitle><description>The impact of direct‐acting antiviral (DAA) therapies on fibrosis regression remains uncertain. In the current study, we prospectively evaluated dynamics of liver stiffness by transient elastography (TE) in patients with chronic HCV infection receiving DAA‐based treatment. Patients (260) were enrolled in the German Hepatitis C‐Registry (DHC‐R), a national multicentre real‐world cohort. Liver stiffness (LS) was assessed at baseline, end of treatment (EOT) and 24 weeks after EOT (FU24) by TE. Biochemical, virological and clinical data were obtained in parallel. In patients with SVR, there was a significant improvement of LS between baseline (median [range], 8.6 [1.7‐73.5] kPa) and FU24 (7.9 [1.7‐75 kPa]; P < .0001) as well as between EOT (8.4 [1.7‐73.5 kPa]) and FU24 [P < .0001]. Stratified by fibrosis stage, patients classified into F4 had higher magnitude of LS reduction between BL (median [range], 25.1 [13.5‐73.5] kPa) and FU24 (21.5 [3.1‐75] kPa; P = .002) compared to those with F2‐F3 (8.9 [7.1‐12.4] kPa and 8.8 [4.2‐29.1]; P = .060) or F0‐F1 (5.3 [1.7‐7] kPa and 5.2 [1.7‐7.7]; P = .064). In cirrhotic patients, low platelets were significantly associated with lack of liver stiffness improvement, both at EOT (P = .018) and at FU24 (P = .012). LS significantly correlated with ALT (r = .371), AST (r = .552), platelets (r = −.499), GGT (r = .250), bilirubin (r = .230), APRI score (r = .512), FIB‐4 score (r = .517) and FORNS index (r = .562); P < .0001. Liver elastography improved significantly in our real‐world cohort after DAA‐based therapy. As LS correlates similarly with transaminase levels and serum fibrosis markers, it might reflect both reduction of necroinflammation and fibrosis regression.</description><subject>Antiviral agents</subject><subject>Antiviral drugs</subject><subject>Bilirubin</subject><subject>chronic hepatitis C</subject><subject>Chronic infection</subject><subject>direct‐acting antiviral (DAA) treatment</subject><subject>Fibrosis</subject><subject>Hepatitis C</subject><subject>Interferon</subject><subject>Liver</subject><subject>Patients</subject><subject>Platelets</subject><subject>Transaminase</subject><subject>transient elastography</subject><issn>1352-0504</issn><issn>1365-2893</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><recordid>eNp1kc1u1DAUhSMEon8seAFkiQ1dpPVPnEmWaAodUKVKFWUbOc71xKPEGXydqbLrI7DgnXiPPgkOU6iEhDe-PufTuZZOkrxm9IzFc77ZtWdM8II-Sw6ZyGXKi1I8n2fJUyppdpAcIW4ojZBkL5MDwWmZC0YPk58Xk1O91UgGQzq7A08wWGMcIJJ6IsErhxZcINApDMPaq207EevIVoVZR3JnQ0t06wdnNWlh1oNFsiQ760eMqAEd7OCIBw12Z92aNDbO4eH-u4pOfCsXouFVR0ILccP0cP_jBnDsYrzxQz_L5BJ8rxxZPW2IATewthj8dJK8MKpDePV4Hye3Hz98Wa7Sq-vLT8v3V6kWUtC0BtXkSvMyUzk0DZhCyqYpFo1ZCKokq4HTgkY7ajU0uqzrTPDSUMn0YiFBHCfv9rlbP3wbAUPVW9TQdcrBMGLFRZ7RTOZ5FtG3_6CbYfQu_q7iGeMFozkTkTrdU9oPiB5MtfW2V36qGK3mdqvYbvW73ci-eUwc6x6av-SfOiNwvgfubAfT_5Oqz19X-8hfbuS3Rw</recordid><startdate>202007</startdate><enddate>202007</enddate><creator>Knop, Viola</creator><creator>Mauss, Stefan</creator><creator>Goeser, Tobias</creator><creator>Geier, Andreas</creator><creator>Zimmermann, Tim</creator><creator>Herzer, 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Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-7434-5218</orcidid></search><sort><creationdate>202007</creationdate><title>Dynamics of liver stiffness by transient elastography in patients with chronic hepatitis C virus infection receiving direct‐acting antiviral therapy—Results from the German Hepatitis C‐Registry</title><author>Knop, Viola ; Mauss, Stefan ; Goeser, Tobias ; Geier, Andreas ; Zimmermann, Tim ; Herzer, Kerstin ; Postel, Nils ; Friedrich‐Rust, Mireen ; Hofmann, Wolf Peter ; Ende, Katrin ; Pathil, Anita ; Bauer, Tilman ; Zeuzem, Stefan ; Berg, Thomas ; Cornberg, Markus ; Börner, Norbert ; Ringelhan, Marc ; Klinker, Hartwig ; Schlenker, Thorsten ; Lutz, Thomas ; Heinzow, Hauke ; Günther, Rainer ; Busch, Heiner ; Baumgarten, Axel ; Buggisch, Peter ; Roessle, Martin ; Hüppe, Dietrich ; Manns, Michael P. ; Niederau, Claus ; Sarrazin, 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Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Knop, Viola</au><au>Mauss, Stefan</au><au>Goeser, Tobias</au><au>Geier, Andreas</au><au>Zimmermann, Tim</au><au>Herzer, Kerstin</au><au>Postel, Nils</au><au>Friedrich‐Rust, Mireen</au><au>Hofmann, Wolf Peter</au><au>Ende, Katrin</au><au>Pathil, Anita</au><au>Bauer, Tilman</au><au>Zeuzem, Stefan</au><au>Berg, Thomas</au><au>Cornberg, Markus</au><au>Börner, Norbert</au><au>Ringelhan, Marc</au><au>Klinker, Hartwig</au><au>Schlenker, Thorsten</au><au>Lutz, Thomas</au><au>Heinzow, Hauke</au><au>Günther, Rainer</au><au>Busch, Heiner</au><au>Baumgarten, Axel</au><au>Buggisch, Peter</au><au>Roessle, Martin</au><au>Hüppe, Dietrich</au><au>Manns, Michael P.</au><au>Niederau, Claus</au><au>Sarrazin, Christoph</au><au>Schirmacher, Peter</au><au>Simon, Karl‐Georg</au><au>Wedemeyer, Heiner</au><aucorp>German Hepatitis C-Registry</aucorp><aucorp>German Hepatitis C‐Registry</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dynamics of liver stiffness by transient elastography in patients with chronic hepatitis C virus infection receiving direct‐acting antiviral therapy—Results from the German Hepatitis C‐Registry</atitle><jtitle>Journal of viral hepatitis</jtitle><addtitle>J Viral Hepat</addtitle><date>2020-07</date><risdate>2020</risdate><volume>27</volume><issue>7</issue><spage>690</spage><epage>698</epage><pages>690-698</pages><issn>1352-0504</issn><eissn>1365-2893</eissn><abstract>The impact of direct‐acting antiviral (DAA) therapies on fibrosis regression remains uncertain. In the current study, we prospectively evaluated dynamics of liver stiffness by transient elastography (TE) in patients with chronic HCV infection receiving DAA‐based treatment. Patients (260) were enrolled in the German Hepatitis C‐Registry (DHC‐R), a national multicentre real‐world cohort. Liver stiffness (LS) was assessed at baseline, end of treatment (EOT) and 24 weeks after EOT (FU24) by TE. Biochemical, virological and clinical data were obtained in parallel. In patients with SVR, there was a significant improvement of LS between baseline (median [range], 8.6 [1.7‐73.5] kPa) and FU24 (7.9 [1.7‐75 kPa]; P < .0001) as well as between EOT (8.4 [1.7‐73.5 kPa]) and FU24 [P < .0001]. Stratified by fibrosis stage, patients classified into F4 had higher magnitude of LS reduction between BL (median [range], 25.1 [13.5‐73.5] kPa) and FU24 (21.5 [3.1‐75] kPa; P = .002) compared to those with F2‐F3 (8.9 [7.1‐12.4] kPa and 8.8 [4.2‐29.1]; P = .060) or F0‐F1 (5.3 [1.7‐7] kPa and 5.2 [1.7‐7.7]; P = .064). In cirrhotic patients, low platelets were significantly associated with lack of liver stiffness improvement, both at EOT (P = .018) and at FU24 (P = .012). LS significantly correlated with ALT (r = .371), AST (r = .552), platelets (r = −.499), GGT (r = .250), bilirubin (r = .230), APRI score (r = .512), FIB‐4 score (r = .517) and FORNS index (r = .562); P < .0001. Liver elastography improved significantly in our real‐world cohort after DAA‐based therapy. As LS correlates similarly with transaminase levels and serum fibrosis markers, it might reflect both reduction of necroinflammation and fibrosis regression.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>32096310</pmid><doi>10.1111/jvh.13280</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-7434-5218</orcidid></addata></record> |
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subjects | Antiviral agents Antiviral drugs Bilirubin chronic hepatitis C Chronic infection direct‐acting antiviral (DAA) treatment Fibrosis Hepatitis C Interferon Liver Patients Platelets Transaminase transient elastography |
title | Dynamics of liver stiffness by transient elastography in patients with chronic hepatitis C virus infection receiving direct‐acting antiviral therapy—Results from the German Hepatitis C‐Registry |
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