Coinfection of hepatitis B and C viruses and risk of hepatocellular carcinoma: Systematic review and meta‐analysis
A subadditive effect of hepatitis B virus (HBV) and hepatitis C virus (HCV) coinfection is possible because superinfection of one virus tends to inhibit infection of the other virus. However, studies have reported inconsistent findings, and two meta‐analyses of studies from various countries (1998)...
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| creator | Cho, Lisa Y. Yang, Jae Jeong Ko, Kwang‐Pil Park, Boyoung Shin, Aesun Lim, Min Kyung Oh, Jin‐Kyoung Park, Sohee Kim, Yoon Jun Shin, Hai‐Rim Yoo, Keun‐Young Park, Sue K. |
| description | A subadditive effect of hepatitis B virus (HBV) and hepatitis C virus (HCV) coinfection is possible because superinfection of one virus tends to inhibit infection of the other virus. However, studies have reported inconsistent findings, and two meta‐analyses of studies from various countries (1998) and China (2005) reported a supraadditive effect for hepatocellular carcinoma (HCC) risk. Thus, we reevaluate HBV/HCV monoinfection and coinfection. Of 411 reports, we included 59 studies that assessed the association between HBV/HCV monoinfection and coinfection for HCC risk. HCC risk because of high/detectable HBV DNA and HBeAg infection was higher than HBsAg infection, whereas anti‐HCV vs anti‐HCV/HCV RNA was not different. Geographically, HCC risk was significantly higher in nonendemic than in HBV or HCV endemic areas. Subadditive effect for HCC risk was presented in recently published studies, cohort studies and studies conducted in HBV/HCV nonendemic areas; an additive effect was presented in studies conducted in HBV endemic areas; a supraadditive effect was presented in previously published studies, case‐control studies and studies conducted in HCV endemic areas. Our results suggest HBV/HCV coinfection for HCC risk is not significantly greater than HBV/HCV monoinfection, and HCC risk due to HBV or HCV is higher in nonendemic than endemic areas. The p‐heterogeneity was significant for most analyses, except HBV(+)/HCV(+) and HBV biomarker analyses. Prevention strategies targeted toward HBV or HCV monoinfected patients are needed. In addition, tailored prevention to reduce infectivity such as HBV markers (HBeAg, HBV DNA) is needed. |
| doi_str_mv | 10.1002/ijc.25321 |
| format | Article |
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However, studies have reported inconsistent findings, and two meta‐analyses of studies from various countries (1998) and China (2005) reported a supraadditive effect for hepatocellular carcinoma (HCC) risk. Thus, we reevaluate HBV/HCV monoinfection and coinfection. Of 411 reports, we included 59 studies that assessed the association between HBV/HCV monoinfection and coinfection for HCC risk. HCC risk because of high/detectable HBV DNA and HBeAg infection was higher than HBsAg infection, whereas anti‐HCV vs anti‐HCV/HCV RNA was not different. Geographically, HCC risk was significantly higher in nonendemic than in HBV or HCV endemic areas. Subadditive effect for HCC risk was presented in recently published studies, cohort studies and studies conducted in HBV/HCV nonendemic areas; an additive effect was presented in studies conducted in HBV endemic areas; a supraadditive effect was presented in previously published studies, case‐control studies and studies conducted in HCV endemic areas. Our results suggest HBV/HCV coinfection for HCC risk is not significantly greater than HBV/HCV monoinfection, and HCC risk due to HBV or HCV is higher in nonendemic than endemic areas. The p‐heterogeneity was significant for most analyses, except HBV(+)/HCV(+) and HBV biomarker analyses. Prevention strategies targeted toward HBV or HCV monoinfected patients are needed. In addition, tailored prevention to reduce infectivity such as HBV markers (HBeAg, HBV DNA) is needed.</description><identifier>ISSN: 0020-7136</identifier><identifier>ISSN: 1097-0215</identifier><identifier>EISSN: 1097-0215</identifier><identifier>DOI: 10.1002/ijc.25321</identifier><identifier>PMID: 20232388</identifier><identifier>CODEN: IJCNAW</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Bioindicators ; Biological and medical sciences ; biomarkers ; Cancer ; Carcinoma, Hepatocellular - epidemiology ; Carcinoma, Hepatocellular - etiology ; China - epidemiology ; DNA ; Gastroenterology. Liver. Pancreas. Abdomen ; Hepatitis ; Hepatitis B ; Hepatitis B - complications ; Hepatitis B - epidemiology ; hepatitis B e antigen ; Hepatitis B surface antigen ; Hepatitis B virus ; Hepatitis C - complications ; Hepatitis C - epidemiology ; Hepatitis C virus ; Hepatocellular carcinoma ; Humans ; infection ; Infectivity ; Korea - epidemiology ; Liver Neoplasms - etiology ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Medical sciences ; meta‐analysis ; prevention ; Reviews ; Risk factors ; RNA ; Spain - epidemiology ; sub‐additive effect ; Superinfection ; Taiwan - epidemiology ; Tumors ; United States - epidemiology ; Viruses</subject><ispartof>International journal of cancer, 2011-01, Vol.128 (1), p.176-184</ispartof><rights>Copyright © 2010 UICC</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2010 UICC.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4881-99e1ecf4e318e0363c8fa97cb89405be90bb2f482a447c4658f76be0e1447a13</citedby><cites>FETCH-LOGICAL-c4881-99e1ecf4e318e0363c8fa97cb89405be90bb2f482a447c4658f76be0e1447a13</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%2Fijc.25321$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fijc.25321$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23783391$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20232388$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cho, Lisa Y.</creatorcontrib><creatorcontrib>Yang, Jae Jeong</creatorcontrib><creatorcontrib>Ko, Kwang‐Pil</creatorcontrib><creatorcontrib>Park, Boyoung</creatorcontrib><creatorcontrib>Shin, Aesun</creatorcontrib><creatorcontrib>Lim, Min Kyung</creatorcontrib><creatorcontrib>Oh, Jin‐Kyoung</creatorcontrib><creatorcontrib>Park, Sohee</creatorcontrib><creatorcontrib>Kim, Yoon Jun</creatorcontrib><creatorcontrib>Shin, Hai‐Rim</creatorcontrib><creatorcontrib>Yoo, Keun‐Young</creatorcontrib><creatorcontrib>Park, Sue K.</creatorcontrib><title>Coinfection of hepatitis B and C viruses and risk of hepatocellular carcinoma: Systematic review and meta‐analysis</title><title>International journal of cancer</title><addtitle>Int J Cancer</addtitle><description>A subadditive effect of hepatitis B virus (HBV) and hepatitis C virus (HCV) coinfection is possible because superinfection of one virus tends to inhibit infection of the other virus. However, studies have reported inconsistent findings, and two meta‐analyses of studies from various countries (1998) and China (2005) reported a supraadditive effect for hepatocellular carcinoma (HCC) risk. Thus, we reevaluate HBV/HCV monoinfection and coinfection. Of 411 reports, we included 59 studies that assessed the association between HBV/HCV monoinfection and coinfection for HCC risk. HCC risk because of high/detectable HBV DNA and HBeAg infection was higher than HBsAg infection, whereas anti‐HCV vs anti‐HCV/HCV RNA was not different. Geographically, HCC risk was significantly higher in nonendemic than in HBV or HCV endemic areas. Subadditive effect for HCC risk was presented in recently published studies, cohort studies and studies conducted in HBV/HCV nonendemic areas; an additive effect was presented in studies conducted in HBV endemic areas; a supraadditive effect was presented in previously published studies, case‐control studies and studies conducted in HCV endemic areas. Our results suggest HBV/HCV coinfection for HCC risk is not significantly greater than HBV/HCV monoinfection, and HCC risk due to HBV or HCV is higher in nonendemic than endemic areas. The p‐heterogeneity was significant for most analyses, except HBV(+)/HCV(+) and HBV biomarker analyses. Prevention strategies targeted toward HBV or HCV monoinfected patients are needed. In addition, tailored prevention to reduce infectivity such as HBV markers (HBeAg, HBV DNA) is needed.</description><subject>Bioindicators</subject><subject>Biological and medical sciences</subject><subject>biomarkers</subject><subject>Cancer</subject><subject>Carcinoma, Hepatocellular - epidemiology</subject><subject>Carcinoma, Hepatocellular - etiology</subject><subject>China - epidemiology</subject><subject>DNA</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Hepatitis</subject><subject>Hepatitis B</subject><subject>Hepatitis B - complications</subject><subject>Hepatitis B - epidemiology</subject><subject>hepatitis B e antigen</subject><subject>Hepatitis B surface antigen</subject><subject>Hepatitis B virus</subject><subject>Hepatitis C - complications</subject><subject>Hepatitis C - epidemiology</subject><subject>Hepatitis C virus</subject><subject>Hepatocellular carcinoma</subject><subject>Humans</subject><subject>infection</subject><subject>Infectivity</subject><subject>Korea - epidemiology</subject><subject>Liver Neoplasms - etiology</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Medical sciences</subject><subject>meta‐analysis</subject><subject>prevention</subject><subject>Reviews</subject><subject>Risk factors</subject><subject>RNA</subject><subject>Spain - epidemiology</subject><subject>sub‐additive effect</subject><subject>Superinfection</subject><subject>Taiwan - epidemiology</subject><subject>Tumors</subject><subject>United States - epidemiology</subject><subject>Viruses</subject><issn>0020-7136</issn><issn>1097-0215</issn><issn>1097-0215</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp90ctu1TAQBmALgehpYdEXQN4gyiKtL0nssIOohaJKLOg-mrhj1SWXgydpdXZ9hD5jn6Q-F8oKVtbI3_xjeRg7lOJYCqFOwo07VoVW8gVbSFGZTChZvGSLdCcyI3W5x_aJboSQshD5a7anhNJKW7tgUz2GwaObwjjw0fNrXMIUpkD8C4fhitf8NsSZkDZVDPTrWY0Ou27uIHIH0YVh7OET_7miCfsU4XjE24B3m74eJ3i8f4ABuhUFesNeeegI3-7OA3Z5dnpZf8sufnw9rz9fZC63VmZVhRKdz1FLi0KX2lkPlXGtrXJRtFiJtlU-twry3Li8LKw3ZYsCZapB6gP2YRu7jOPvGWlq-kDrR8OA40yNKVVqFsokefRfKYU0VVlaqRL9uKUujkQRfbOMoYe4SqhZb6NJ22g220j23S52bnu8epZ_vj-B9zsA5KDzEQYX6K_TxmpdrYNOtu4udLj698Tm_Hu9Hf0EB5Ghsg</recordid><startdate>20110101</startdate><enddate>20110101</enddate><creator>Cho, Lisa Y.</creator><creator>Yang, Jae Jeong</creator><creator>Ko, Kwang‐Pil</creator><creator>Park, Boyoung</creator><creator>Shin, Aesun</creator><creator>Lim, Min Kyung</creator><creator>Oh, Jin‐Kyoung</creator><creator>Park, Sohee</creator><creator>Kim, Yoon Jun</creator><creator>Shin, Hai‐Rim</creator><creator>Yoo, Keun‐Young</creator><creator>Park, Sue K.</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Blackwell</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>7U1</scope><scope>7U2</scope><scope>7U9</scope><scope>C1K</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>20110101</creationdate><title>Coinfection of hepatitis B and C viruses and risk of hepatocellular carcinoma: Systematic review and meta‐analysis</title><author>Cho, Lisa Y. ; Yang, Jae Jeong ; Ko, Kwang‐Pil ; Park, Boyoung ; Shin, Aesun ; Lim, Min Kyung ; Oh, Jin‐Kyoung ; Park, Sohee ; Kim, Yoon Jun ; Shin, Hai‐Rim ; Yoo, Keun‐Young ; Park, Sue K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4881-99e1ecf4e318e0363c8fa97cb89405be90bb2f482a447c4658f76be0e1447a13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Bioindicators</topic><topic>Biological and medical sciences</topic><topic>biomarkers</topic><topic>Cancer</topic><topic>Carcinoma, Hepatocellular - epidemiology</topic><topic>Carcinoma, Hepatocellular - etiology</topic><topic>China - epidemiology</topic><topic>DNA</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Hepatitis</topic><topic>Hepatitis B</topic><topic>Hepatitis B - complications</topic><topic>Hepatitis B - epidemiology</topic><topic>hepatitis B e antigen</topic><topic>Hepatitis B surface antigen</topic><topic>Hepatitis B virus</topic><topic>Hepatitis C - complications</topic><topic>Hepatitis C - epidemiology</topic><topic>Hepatitis C virus</topic><topic>Hepatocellular carcinoma</topic><topic>Humans</topic><topic>infection</topic><topic>Infectivity</topic><topic>Korea - epidemiology</topic><topic>Liver Neoplasms - etiology</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Medical sciences</topic><topic>meta‐analysis</topic><topic>prevention</topic><topic>Reviews</topic><topic>Risk factors</topic><topic>RNA</topic><topic>Spain - epidemiology</topic><topic>sub‐additive effect</topic><topic>Superinfection</topic><topic>Taiwan - epidemiology</topic><topic>Tumors</topic><topic>United States - epidemiology</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cho, Lisa Y.</creatorcontrib><creatorcontrib>Yang, Jae Jeong</creatorcontrib><creatorcontrib>Ko, Kwang‐Pil</creatorcontrib><creatorcontrib>Park, Boyoung</creatorcontrib><creatorcontrib>Shin, Aesun</creatorcontrib><creatorcontrib>Lim, Min Kyung</creatorcontrib><creatorcontrib>Oh, Jin‐Kyoung</creatorcontrib><creatorcontrib>Park, Sohee</creatorcontrib><creatorcontrib>Kim, Yoon Jun</creatorcontrib><creatorcontrib>Shin, Hai‐Rim</creatorcontrib><creatorcontrib>Yoo, Keun‐Young</creatorcontrib><creatorcontrib>Park, Sue K.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Risk Abstracts</collection><collection>Safety Science and Risk</collection><collection>Virology and AIDS Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cho, Lisa Y.</au><au>Yang, Jae Jeong</au><au>Ko, Kwang‐Pil</au><au>Park, Boyoung</au><au>Shin, Aesun</au><au>Lim, Min Kyung</au><au>Oh, Jin‐Kyoung</au><au>Park, Sohee</au><au>Kim, Yoon Jun</au><au>Shin, Hai‐Rim</au><au>Yoo, Keun‐Young</au><au>Park, Sue K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Coinfection of hepatitis B and C viruses and risk of hepatocellular carcinoma: Systematic review and meta‐analysis</atitle><jtitle>International journal of cancer</jtitle><addtitle>Int J Cancer</addtitle><date>2011-01-01</date><risdate>2011</risdate><volume>128</volume><issue>1</issue><spage>176</spage><epage>184</epage><pages>176-184</pages><issn>0020-7136</issn><issn>1097-0215</issn><eissn>1097-0215</eissn><coden>IJCNAW</coden><abstract>A subadditive effect of hepatitis B virus (HBV) and hepatitis C virus (HCV) coinfection is possible because superinfection of one virus tends to inhibit infection of the other virus. However, studies have reported inconsistent findings, and two meta‐analyses of studies from various countries (1998) and China (2005) reported a supraadditive effect for hepatocellular carcinoma (HCC) risk. Thus, we reevaluate HBV/HCV monoinfection and coinfection. Of 411 reports, we included 59 studies that assessed the association between HBV/HCV monoinfection and coinfection for HCC risk. HCC risk because of high/detectable HBV DNA and HBeAg infection was higher than HBsAg infection, whereas anti‐HCV vs anti‐HCV/HCV RNA was not different. Geographically, HCC risk was significantly higher in nonendemic than in HBV or HCV endemic areas. Subadditive effect for HCC risk was presented in recently published studies, cohort studies and studies conducted in HBV/HCV nonendemic areas; an additive effect was presented in studies conducted in HBV endemic areas; a supraadditive effect was presented in previously published studies, case‐control studies and studies conducted in HCV endemic areas. Our results suggest HBV/HCV coinfection for HCC risk is not significantly greater than HBV/HCV monoinfection, and HCC risk due to HBV or HCV is higher in nonendemic than endemic areas. The p‐heterogeneity was significant for most analyses, except HBV(+)/HCV(+) and HBV biomarker analyses. Prevention strategies targeted toward HBV or HCV monoinfected patients are needed. In addition, tailored prevention to reduce infectivity such as HBV markers (HBeAg, HBV DNA) is needed.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>20232388</pmid><doi>10.1002/ijc.25321</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Bioindicators Biological and medical sciences biomarkers Cancer Carcinoma, Hepatocellular - epidemiology Carcinoma, Hepatocellular - etiology China - epidemiology DNA Gastroenterology. Liver. Pancreas. Abdomen Hepatitis Hepatitis B Hepatitis B - complications Hepatitis B - epidemiology hepatitis B e antigen Hepatitis B surface antigen Hepatitis B virus Hepatitis C - complications Hepatitis C - epidemiology Hepatitis C virus Hepatocellular carcinoma Humans infection Infectivity Korea - epidemiology Liver Neoplasms - etiology Liver. Biliary tract. Portal circulation. Exocrine pancreas Medical sciences meta‐analysis prevention Reviews Risk factors RNA Spain - epidemiology sub‐additive effect Superinfection Taiwan - epidemiology Tumors United States - epidemiology Viruses |
| title | Coinfection of hepatitis B and C viruses and risk of hepatocellular carcinoma: Systematic review and meta‐analysis |
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