Impact of Serial Hepatitis B Virus DNA on Hepatocellular Carcinoma Development in Patients with Liver Cirrhosis
Objectives: We investigated the pattern of serial HBV DNA levels in known cirrhosis patients and its impact on the development of hepatocellular carcinoma (HCC). Methods: We analyzed a retrospective case/control study based on 352 HCC patients associated with HBV between 2005 and 2007. Prior to HCC...
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| Veröffentlicht in: | Intervirology 2010-01, Vol.53 (2), p.111-118 |
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| creator | Kwon, Jung Hyun Choi, Jong Young Jang, Jeong Won Bae, Si Hyun Yoon, Seung Kew Yang, Jin Mo Han, Nam Ik Lee, Chang Don Lee, Young Seok Chung, Kyu Won |
| description | Objectives: We investigated the pattern of serial HBV DNA levels in known cirrhosis patients and its impact on the development of hepatocellular carcinoma (HCC). Methods: We analyzed a retrospective case/control study based on 352 HCC patients associated with HBV between 2005 and 2007. Prior to HCC development, 49 cirrhosis patients were tested for HBV DNA levels more than once a year (median 4 times) during the follow-up period. Ninety-eight consecutive cirrhosis patients without HCC, matched for age, sex and HBe Ag status were included as controls. Eighty-three patients in both groups had undergone antiviral therapy. Results: In cirrhosis, the most common HBV DNA pattern was fluctuating (33.3%), followed by persistently high (≧10 4 copies/ml, 23.8%). Compared to a persistently low pattern ( |
| doi_str_mv | 10.1159/000264201 |
| format | Article |
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Methods: We analyzed a retrospective case/control study based on 352 HCC patients associated with HBV between 2005 and 2007. Prior to HCC development, 49 cirrhosis patients were tested for HBV DNA levels more than once a year (median 4 times) during the follow-up period. Ninety-eight consecutive cirrhosis patients without HCC, matched for age, sex and HBe Ag status were included as controls. Eighty-three patients in both groups had undergone antiviral therapy. Results: In cirrhosis, the most common HBV DNA pattern was fluctuating (33.3%), followed by persistently high (≧10 4 copies/ml, 23.8%). Compared to a persistently low pattern (<10 4 copies/ml), the relative risks of HCC in patients with persistently high and fluctuating patterns were 2.650 and 1.475. At multivariate analysis, a persistently high pattern was an independent risk factor for HCC (hazard ratio 3.135). Patients with sustained HBV DNA suppression during antiviral therapy were less likely to develop HCC than those with viral breakthrough/nonresponse. Conclusions: This study showed that persistent suppression of HBV DNA is also important to prevent the development of HCC in known cirrhosis patients.</description><identifier>ISSN: 0300-5526</identifier><identifier>EISSN: 1423-0100</identifier><identifier>DOI: 10.1159/000264201</identifier><identifier>PMID: 19955816</identifier><identifier>CODEN: IVRYAK</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Aged ; Antiviral Agents - therapeutic use ; Carcinoma, Hepatocellular - virology ; Case-Control Studies ; DNA, Viral - blood ; Female ; Hepatitis B virus ; Hepatitis B virus - isolation & purification ; Hepatitis B, Chronic - complications ; Hepatitis B, Chronic - drug therapy ; Hepatitis B, Chronic - virology ; Humans ; Liver Cirrhosis - complications ; Liver Cirrhosis - virology ; Male ; Middle Aged ; Original Paper ; Retrospective Studies ; Viral Load</subject><ispartof>Intervirology, 2010-01, Vol.53 (2), p.111-118</ispartof><rights>2009 S. Karger AG, Basel</rights><rights>Copyright 2009 S. Karger AG, Basel.</rights><rights>Copyright (c) 2010 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c398t-e2d1907a2519321186346c7b024a0813918e17224de02a0452d22bfe6d4d3e153</citedby><cites>FETCH-LOGICAL-c398t-e2d1907a2519321186346c7b024a0813918e17224de02a0452d22bfe6d4d3e153</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,2427,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19955816$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kwon, Jung Hyun</creatorcontrib><creatorcontrib>Choi, Jong Young</creatorcontrib><creatorcontrib>Jang, Jeong Won</creatorcontrib><creatorcontrib>Bae, Si Hyun</creatorcontrib><creatorcontrib>Yoon, Seung Kew</creatorcontrib><creatorcontrib>Yang, Jin Mo</creatorcontrib><creatorcontrib>Han, Nam Ik</creatorcontrib><creatorcontrib>Lee, Chang Don</creatorcontrib><creatorcontrib>Lee, Young Seok</creatorcontrib><creatorcontrib>Chung, Kyu Won</creatorcontrib><title>Impact of Serial Hepatitis B Virus DNA on Hepatocellular Carcinoma Development in Patients with Liver Cirrhosis</title><title>Intervirology</title><addtitle>Intervirology</addtitle><description>Objectives: We investigated the pattern of serial HBV DNA levels in known cirrhosis patients and its impact on the development of hepatocellular carcinoma (HCC). Methods: We analyzed a retrospective case/control study based on 352 HCC patients associated with HBV between 2005 and 2007. Prior to HCC development, 49 cirrhosis patients were tested for HBV DNA levels more than once a year (median 4 times) during the follow-up period. Ninety-eight consecutive cirrhosis patients without HCC, matched for age, sex and HBe Ag status were included as controls. Eighty-three patients in both groups had undergone antiviral therapy. Results: In cirrhosis, the most common HBV DNA pattern was fluctuating (33.3%), followed by persistently high (≧10 4 copies/ml, 23.8%). Compared to a persistently low pattern (<10 4 copies/ml), the relative risks of HCC in patients with persistently high and fluctuating patterns were 2.650 and 1.475. At multivariate analysis, a persistently high pattern was an independent risk factor for HCC (hazard ratio 3.135). Patients with sustained HBV DNA suppression during antiviral therapy were less likely to develop HCC than those with viral breakthrough/nonresponse. Conclusions: This study showed that persistent suppression of HBV DNA is also important to prevent the development of HCC in known cirrhosis patients.</description><subject>Aged</subject><subject>Antiviral Agents - therapeutic use</subject><subject>Carcinoma, Hepatocellular - virology</subject><subject>Case-Control Studies</subject><subject>DNA, Viral - blood</subject><subject>Female</subject><subject>Hepatitis B virus</subject><subject>Hepatitis B virus - isolation & purification</subject><subject>Hepatitis B, Chronic - complications</subject><subject>Hepatitis B, Chronic - drug therapy</subject><subject>Hepatitis B, Chronic - virology</subject><subject>Humans</subject><subject>Liver Cirrhosis - complications</subject><subject>Liver Cirrhosis - virology</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Original Paper</subject><subject>Retrospective Studies</subject><subject>Viral Load</subject><issn>0300-5526</issn><issn>1423-0100</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp90U1v1DAQBmALUdFl4cAdIYsDqIfAzNj58LFsgVZaFSRor5E3maUuSRzspIh_j6tdtVIPPXkkPzMa-xXiFcIHxNx8BAAqNAE-EQvUpDJAgKdiAQogy3MqDsXzGK8TU6jgmThEY_K8wmIh_Fk_2maSfit_cHC2k6c82slNLspP8tKFOcqT82Pph92Fb7jr5s4GubKhcYPvrTzhG-782PMwSTfI76k9lVH-ddOVXLsbTtiFcOWjiy_EwdZ2kV_uz6W4-PL55-o0W3_7erY6XmeNMtWUMbVooLSUo1GEWBVKF025AdIWKlQGK8aSSLcMZEHn1BJttly0ulWMuVqK97u5Y_B_Zo5T3bt4u7sd2M-xLpWqKjTps5bi3aOSUGFpoEjw7QN47ecwpFfUBBq1KgkSOtqhJvgYA2_rMbjehn81Qn0bVn0XVrJv9gPnTc_tvdynk8DrHfhtwy8Od2Df_x8qcJT8</recordid><startdate>20100101</startdate><enddate>20100101</enddate><creator>Kwon, Jung Hyun</creator><creator>Choi, Jong Young</creator><creator>Jang, Jeong Won</creator><creator>Bae, Si Hyun</creator><creator>Yoon, Seung Kew</creator><creator>Yang, Jin Mo</creator><creator>Han, Nam Ik</creator><creator>Lee, Chang Don</creator><creator>Lee, Young Seok</creator><creator>Chung, Kyu Won</creator><general>S. 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therapeutic use</topic><topic>Carcinoma, Hepatocellular - virology</topic><topic>Case-Control Studies</topic><topic>DNA, Viral - blood</topic><topic>Female</topic><topic>Hepatitis B virus</topic><topic>Hepatitis B virus - isolation & purification</topic><topic>Hepatitis B, Chronic - complications</topic><topic>Hepatitis B, Chronic - drug therapy</topic><topic>Hepatitis B, Chronic - virology</topic><topic>Humans</topic><topic>Liver Cirrhosis - complications</topic><topic>Liver Cirrhosis - virology</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Original Paper</topic><topic>Retrospective Studies</topic><topic>Viral Load</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kwon, Jung Hyun</creatorcontrib><creatorcontrib>Choi, Jong Young</creatorcontrib><creatorcontrib>Jang, Jeong Won</creatorcontrib><creatorcontrib>Bae, Si Hyun</creatorcontrib><creatorcontrib>Yoon, Seung Kew</creatorcontrib><creatorcontrib>Yang, Jin Mo</creatorcontrib><creatorcontrib>Han, Nam Ik</creatorcontrib><creatorcontrib>Lee, Chang Don</creatorcontrib><creatorcontrib>Lee, Young Seok</creatorcontrib><creatorcontrib>Chung, Kyu Won</creatorcontrib><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>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</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 Pharma Collection</collection><collection>Technology Research 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>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</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>Biotechnology and BioEngineering Abstracts</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 Basic</collection><collection>Genetics Abstracts</collection><collection>SIRS Editorial</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><jtitle>Intervirology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kwon, Jung Hyun</au><au>Choi, Jong Young</au><au>Jang, Jeong Won</au><au>Bae, Si Hyun</au><au>Yoon, Seung Kew</au><au>Yang, Jin Mo</au><au>Han, Nam Ik</au><au>Lee, Chang Don</au><au>Lee, Young Seok</au><au>Chung, Kyu Won</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Impact of Serial Hepatitis B Virus DNA on Hepatocellular Carcinoma Development in Patients with Liver Cirrhosis</atitle><jtitle>Intervirology</jtitle><addtitle>Intervirology</addtitle><date>2010-01-01</date><risdate>2010</risdate><volume>53</volume><issue>2</issue><spage>111</spage><epage>118</epage><pages>111-118</pages><issn>0300-5526</issn><eissn>1423-0100</eissn><coden>IVRYAK</coden><abstract>Objectives: We investigated the pattern of serial HBV DNA levels in known cirrhosis patients and its impact on the development of hepatocellular carcinoma (HCC). Methods: We analyzed a retrospective case/control study based on 352 HCC patients associated with HBV between 2005 and 2007. Prior to HCC development, 49 cirrhosis patients were tested for HBV DNA levels more than once a year (median 4 times) during the follow-up period. Ninety-eight consecutive cirrhosis patients without HCC, matched for age, sex and HBe Ag status were included as controls. Eighty-three patients in both groups had undergone antiviral therapy. Results: In cirrhosis, the most common HBV DNA pattern was fluctuating (33.3%), followed by persistently high (≧10 4 copies/ml, 23.8%). Compared to a persistently low pattern (<10 4 copies/ml), the relative risks of HCC in patients with persistently high and fluctuating patterns were 2.650 and 1.475. At multivariate analysis, a persistently high pattern was an independent risk factor for HCC (hazard ratio 3.135). Patients with sustained HBV DNA suppression during antiviral therapy were less likely to develop HCC than those with viral breakthrough/nonresponse. Conclusions: This study showed that persistent suppression of HBV DNA is also important to prevent the development of HCC in known cirrhosis patients.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>19955816</pmid><doi>10.1159/000264201</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Aged Antiviral Agents - therapeutic use Carcinoma, Hepatocellular - virology Case-Control Studies DNA, Viral - blood Female Hepatitis B virus Hepatitis B virus - isolation & purification Hepatitis B, Chronic - complications Hepatitis B, Chronic - drug therapy Hepatitis B, Chronic - virology Humans Liver Cirrhosis - complications Liver Cirrhosis - virology Male Middle Aged Original Paper Retrospective Studies Viral Load |
| title | Impact of Serial Hepatitis B Virus DNA on Hepatocellular Carcinoma Development in Patients with Liver Cirrhosis |
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