Pre-S Deletion and Complex Mutations of Hepatitis B Virus Related to Advanced Liver Disease in HBeAg-Negative Patients
Background & Aims: This longitudinal study investigated the interactions and roles of hepatitis B virus (HBV) genotypes, pre-S deletions, and core promoter and precore mutations on the progression of liver disease in hepatitis B e antigen (HBeAg)-negative patients. Methods: A total of 141 HBeAg-...
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Veröffentlicht in: | Gastroenterology (New York, N.Y. 1943) N.Y. 1943), 2007-11, Vol.133 (5), p.1466-1474 |
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container_title | Gastroenterology (New York, N.Y. 1943) |
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creator | Chen, Chien–Hung Hung, Chao–Hung Lee, Chuan–Mo Hu, Tsung–Hui Wang, Jing–Houng Wang, Jyh–Chwan Lu, Sheng–Nan Changchien, Chi–Sin |
description | Background & Aims: This longitudinal study investigated the interactions and roles of hepatitis B virus (HBV) genotypes, pre-S deletions, and core promoter and precore mutations on the progression of liver disease in hepatitis B e antigen (HBeAg)-negative patients. Methods: A total of 141 HBeAg-negative patients without liver cirrhosis or hepatocellular carcinoma at study entry were recruited for this study, including 45 inactive HBV carriers and 96 patients with HBeAg-negative chronic hepatitis B. The HBV genotypes and the sequences of pre-S, core promoter, and precore regions were determined. Results: Compared with patients without developing liver cirrhosis, patients with the development of liver cirrhosis had higher rates of genotype C; pre-S deletions; C or G1753, T1762/A1764, T1766, and/or A1768 mutants; and G1799 variant. Cox regression analysis showed that older age, higher total bilirubin and HBV DNA levels, pre-S deletions, and T1766 and/or A1768 mutants were significantly associated with the development of liver cirrhosis. HBV with a complex mutation pattern (pre-S deletion, T1762/A1764, and T1766 and/or A1768 mutants) rather than a single mutation was associated with the development of liver cirrhosis, and the patterns of mutation combinations differed between HBV genotype B and C. Moreover, pre-S deletion was a significant risk factor for hepatocellular carcinoma. Conclusions: This study indicated that pre-S deletion and combined mutations of HBV are useful molecular markers for predicting the clinical outcomes of HBeAg-negative patients. |
doi_str_mv | 10.1053/j.gastro.2007.09.002 |
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Methods: A total of 141 HBeAg-negative patients without liver cirrhosis or hepatocellular carcinoma at study entry were recruited for this study, including 45 inactive HBV carriers and 96 patients with HBeAg-negative chronic hepatitis B. The HBV genotypes and the sequences of pre-S, core promoter, and precore regions were determined. Results: Compared with patients without developing liver cirrhosis, patients with the development of liver cirrhosis had higher rates of genotype C; pre-S deletions; C or G1753, T1762/A1764, T1766, and/or A1768 mutants; and G1799 variant. Cox regression analysis showed that older age, higher total bilirubin and HBV DNA levels, pre-S deletions, and T1766 and/or A1768 mutants were significantly associated with the development of liver cirrhosis. HBV with a complex mutation pattern (pre-S deletion, T1762/A1764, and T1766 and/or A1768 mutants) rather than a single mutation was associated with the development of liver cirrhosis, and the patterns of mutation combinations differed between HBV genotype B and C. Moreover, pre-S deletion was a significant risk factor for hepatocellular carcinoma. Conclusions: This study indicated that pre-S deletion and combined mutations of HBV are useful molecular markers for predicting the clinical outcomes of HBeAg-negative patients.</description><identifier>ISSN: 0016-5085</identifier><identifier>EISSN: 1528-0012</identifier><identifier>DOI: 10.1053/j.gastro.2007.09.002</identifier><identifier>PMID: 17915220</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adult ; Bilirubin - blood ; Carcinoma, Hepatocellular - etiology ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - immunology ; Disease Progression ; DNA, Viral - blood ; Female ; Gastroenterology and Hepatology ; Gene Deletion ; Genotype ; Hepatitis B - complications ; Hepatitis B - genetics ; Hepatitis B - immunology ; Hepatitis B e Antigens - blood ; Hepatitis B Surface Antigens - genetics ; Hepatitis B virus - genetics ; Hepatitis B virus - immunology ; Humans ; Liver Cirrhosis - etiology ; Liver Cirrhosis - genetics ; Liver Cirrhosis - immunology ; Liver Neoplasms - etiology ; Liver Neoplasms - genetics ; Liver Neoplasms - immunology ; Longitudinal Studies ; Male ; Middle Aged ; Mutation - genetics ; Predictive Value of Tests ; Protein Precursors - genetics ; Regression Analysis ; Viral Core Proteins - genetics</subject><ispartof>Gastroenterology (New York, N.Y. 1943), 2007-11, Vol.133 (5), p.1466-1474</ispartof><rights>AGA Institute</rights><rights>2007 AGA Institute</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c415t-c502d60dc7697cae6ff0afda4a2a5cbad98b463bffdab04efdbd97ada5cad84e3</citedby><cites>FETCH-LOGICAL-c415t-c502d60dc7697cae6ff0afda4a2a5cbad98b463bffdab04efdbd97ada5cad84e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1053/j.gastro.2007.09.002$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17915220$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Chien–Hung</creatorcontrib><creatorcontrib>Hung, Chao–Hung</creatorcontrib><creatorcontrib>Lee, Chuan–Mo</creatorcontrib><creatorcontrib>Hu, Tsung–Hui</creatorcontrib><creatorcontrib>Wang, Jing–Houng</creatorcontrib><creatorcontrib>Wang, Jyh–Chwan</creatorcontrib><creatorcontrib>Lu, Sheng–Nan</creatorcontrib><creatorcontrib>Changchien, Chi–Sin</creatorcontrib><title>Pre-S Deletion and Complex Mutations of Hepatitis B Virus Related to Advanced Liver Disease in HBeAg-Negative Patients</title><title>Gastroenterology (New York, N.Y. 1943)</title><addtitle>Gastroenterology</addtitle><description>Background & Aims: This longitudinal study investigated the interactions and roles of hepatitis B virus (HBV) genotypes, pre-S deletions, and core promoter and precore mutations on the progression of liver disease in hepatitis B e antigen (HBeAg)-negative patients. Methods: A total of 141 HBeAg-negative patients without liver cirrhosis or hepatocellular carcinoma at study entry were recruited for this study, including 45 inactive HBV carriers and 96 patients with HBeAg-negative chronic hepatitis B. The HBV genotypes and the sequences of pre-S, core promoter, and precore regions were determined. Results: Compared with patients without developing liver cirrhosis, patients with the development of liver cirrhosis had higher rates of genotype C; pre-S deletions; C or G1753, T1762/A1764, T1766, and/or A1768 mutants; and G1799 variant. Cox regression analysis showed that older age, higher total bilirubin and HBV DNA levels, pre-S deletions, and T1766 and/or A1768 mutants were significantly associated with the development of liver cirrhosis. HBV with a complex mutation pattern (pre-S deletion, T1762/A1764, and T1766 and/or A1768 mutants) rather than a single mutation was associated with the development of liver cirrhosis, and the patterns of mutation combinations differed between HBV genotype B and C. Moreover, pre-S deletion was a significant risk factor for hepatocellular carcinoma. Conclusions: This study indicated that pre-S deletion and combined mutations of HBV are useful molecular markers for predicting the clinical outcomes of HBeAg-negative patients.</description><subject>Adult</subject><subject>Bilirubin - blood</subject><subject>Carcinoma, Hepatocellular - etiology</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carcinoma, Hepatocellular - immunology</subject><subject>Disease Progression</subject><subject>DNA, Viral - blood</subject><subject>Female</subject><subject>Gastroenterology and Hepatology</subject><subject>Gene Deletion</subject><subject>Genotype</subject><subject>Hepatitis B - complications</subject><subject>Hepatitis B - genetics</subject><subject>Hepatitis B - immunology</subject><subject>Hepatitis B e Antigens - blood</subject><subject>Hepatitis B Surface Antigens - genetics</subject><subject>Hepatitis B virus - genetics</subject><subject>Hepatitis B virus - immunology</subject><subject>Humans</subject><subject>Liver Cirrhosis - etiology</subject><subject>Liver Cirrhosis - genetics</subject><subject>Liver Cirrhosis - immunology</subject><subject>Liver Neoplasms - etiology</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - immunology</subject><subject>Longitudinal Studies</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Mutation - genetics</subject><subject>Predictive Value of Tests</subject><subject>Protein Precursors - genetics</subject><subject>Regression Analysis</subject><subject>Viral Core Proteins - genetics</subject><issn>0016-5085</issn><issn>1528-0012</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU-P0zAQxS0EYsvCN0DIJ24J4_zPBanbBYpUYMUCV8uxJ5VLGhePE7HfHkethMSF0xuP3zzLv2HspYBUQJm_OaR7RcG7NAOoU2hTgOwRW4kyaxIAkT1mqyhVUkJTXrFnRAcAaPNGPGVXom6jL4MVm-88Jvf8FgcM1o1cjYZv3PE04G_-aQpqaRJ3Pd_iKR6CJX7Df1g_Ef-KgwpoeHB8bWY16ljv7Iye31pCRcjtyLc3uN4nn3Efh2fkd1FwDPScPenVQPjiotfs-_t33zbbZPflw8fNepfoQpQh0SVkpgKj66qttcKq70H1RhUqU6XulGmbrqjyro-9DgrsTWfaWpl4qUxTYH7NXp9zT979mpCCPFrSOAxqRDeRrJqibqq8jcbibNTeEXns5cnbo_IPUoBceMuDPPOWC28JrYy849irS_7UHdH8HboAjoa3ZwPGX84WvSQdCURW1qMO0jj7vxf-DdCDHa1Ww098QDq4yY-RoBSSMgnyftn5snKoY1HkZf4HEHuqaw</recordid><startdate>20071101</startdate><enddate>20071101</enddate><creator>Chen, Chien–Hung</creator><creator>Hung, Chao–Hung</creator><creator>Lee, Chuan–Mo</creator><creator>Hu, Tsung–Hui</creator><creator>Wang, Jing–Houng</creator><creator>Wang, Jyh–Chwan</creator><creator>Lu, Sheng–Nan</creator><creator>Changchien, Chi–Sin</creator><general>Elsevier Inc</general><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>7X8</scope></search><sort><creationdate>20071101</creationdate><title>Pre-S Deletion and Complex Mutations of Hepatitis B Virus Related to Advanced Liver Disease in HBeAg-Negative Patients</title><author>Chen, Chien–Hung ; Hung, Chao–Hung ; Lee, Chuan–Mo ; Hu, Tsung–Hui ; Wang, Jing–Houng ; Wang, Jyh–Chwan ; Lu, Sheng–Nan ; Changchien, Chi–Sin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c415t-c502d60dc7697cae6ff0afda4a2a5cbad98b463bffdab04efdbd97ada5cad84e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adult</topic><topic>Bilirubin - blood</topic><topic>Carcinoma, Hepatocellular - etiology</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Carcinoma, Hepatocellular - immunology</topic><topic>Disease Progression</topic><topic>DNA, Viral - blood</topic><topic>Female</topic><topic>Gastroenterology and Hepatology</topic><topic>Gene Deletion</topic><topic>Genotype</topic><topic>Hepatitis B - complications</topic><topic>Hepatitis B - genetics</topic><topic>Hepatitis B - immunology</topic><topic>Hepatitis B e Antigens - blood</topic><topic>Hepatitis B Surface Antigens - genetics</topic><topic>Hepatitis B virus - genetics</topic><topic>Hepatitis B virus - immunology</topic><topic>Humans</topic><topic>Liver Cirrhosis - etiology</topic><topic>Liver Cirrhosis - genetics</topic><topic>Liver Cirrhosis - immunology</topic><topic>Liver Neoplasms - etiology</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - immunology</topic><topic>Longitudinal Studies</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Mutation - genetics</topic><topic>Predictive Value of Tests</topic><topic>Protein Precursors - genetics</topic><topic>Regression Analysis</topic><topic>Viral Core Proteins - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen, Chien–Hung</creatorcontrib><creatorcontrib>Hung, Chao–Hung</creatorcontrib><creatorcontrib>Lee, Chuan–Mo</creatorcontrib><creatorcontrib>Hu, Tsung–Hui</creatorcontrib><creatorcontrib>Wang, Jing–Houng</creatorcontrib><creatorcontrib>Wang, Jyh–Chwan</creatorcontrib><creatorcontrib>Lu, Sheng–Nan</creatorcontrib><creatorcontrib>Changchien, Chi–Sin</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Gastroenterology (New York, N.Y. 1943)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Chien–Hung</au><au>Hung, Chao–Hung</au><au>Lee, Chuan–Mo</au><au>Hu, Tsung–Hui</au><au>Wang, Jing–Houng</au><au>Wang, Jyh–Chwan</au><au>Lu, Sheng–Nan</au><au>Changchien, Chi–Sin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pre-S Deletion and Complex Mutations of Hepatitis B Virus Related to Advanced Liver Disease in HBeAg-Negative Patients</atitle><jtitle>Gastroenterology (New York, N.Y. 1943)</jtitle><addtitle>Gastroenterology</addtitle><date>2007-11-01</date><risdate>2007</risdate><volume>133</volume><issue>5</issue><spage>1466</spage><epage>1474</epage><pages>1466-1474</pages><issn>0016-5085</issn><eissn>1528-0012</eissn><abstract>Background & Aims: This longitudinal study investigated the interactions and roles of hepatitis B virus (HBV) genotypes, pre-S deletions, and core promoter and precore mutations on the progression of liver disease in hepatitis B e antigen (HBeAg)-negative patients. Methods: A total of 141 HBeAg-negative patients without liver cirrhosis or hepatocellular carcinoma at study entry were recruited for this study, including 45 inactive HBV carriers and 96 patients with HBeAg-negative chronic hepatitis B. The HBV genotypes and the sequences of pre-S, core promoter, and precore regions were determined. Results: Compared with patients without developing liver cirrhosis, patients with the development of liver cirrhosis had higher rates of genotype C; pre-S deletions; C or G1753, T1762/A1764, T1766, and/or A1768 mutants; and G1799 variant. Cox regression analysis showed that older age, higher total bilirubin and HBV DNA levels, pre-S deletions, and T1766 and/or A1768 mutants were significantly associated with the development of liver cirrhosis. HBV with a complex mutation pattern (pre-S deletion, T1762/A1764, and T1766 and/or A1768 mutants) rather than a single mutation was associated with the development of liver cirrhosis, and the patterns of mutation combinations differed between HBV genotype B and C. Moreover, pre-S deletion was a significant risk factor for hepatocellular carcinoma. Conclusions: This study indicated that pre-S deletion and combined mutations of HBV are useful molecular markers for predicting the clinical outcomes of HBeAg-negative patients.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>17915220</pmid><doi>10.1053/j.gastro.2007.09.002</doi><tpages>9</tpages></addata></record> |
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subjects | Adult Bilirubin - blood Carcinoma, Hepatocellular - etiology Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - immunology Disease Progression DNA, Viral - blood Female Gastroenterology and Hepatology Gene Deletion Genotype Hepatitis B - complications Hepatitis B - genetics Hepatitis B - immunology Hepatitis B e Antigens - blood Hepatitis B Surface Antigens - genetics Hepatitis B virus - genetics Hepatitis B virus - immunology Humans Liver Cirrhosis - etiology Liver Cirrhosis - genetics Liver Cirrhosis - immunology Liver Neoplasms - etiology Liver Neoplasms - genetics Liver Neoplasms - immunology Longitudinal Studies Male Middle Aged Mutation - genetics Predictive Value of Tests Protein Precursors - genetics Regression Analysis Viral Core Proteins - genetics |
title | Pre-S Deletion and Complex Mutations of Hepatitis B Virus Related to Advanced Liver Disease in HBeAg-Negative Patients |
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