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Article: Impact of precore and core promoter mutations on hepatic histology in patients with chronic hepatitis B

TitleImpact of precore and core promoter mutations on hepatic histology in patients with chronic hepatitis B
Authors
Issue Date2005
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/APT
Citation
Alimentary Pharmacology And Therapeutics, 2005, v. 22 n. 4, p. 301-307 How to Cite?
AbstractBackground: The details of liver histology of patients with precore and core promoter mutations are still not clear. Aim: To determine the role of precore and core promoter mutations in liver histology in Chinese patients with chronic hepatitis B. Patients and methods: Intrahepatic hepatitis B virus DNA (by COBAS Amplicor hepatitis B virus Monitor test) and precore and core promoter mutations (by a line probe assay) were measured in 54 chronic hepatitis B patients. Expression of hepatitis B core antigen, hepatitis B e antigen and hepatitis B surface antigen was determined by immunohistological staining. Histological activity index was scored according to Knodell's criteria. Results: Compared with patients without core promoter mutations, patients with core promoter mutations had more severe intrahepatic inflammation and fibrosis, and more cytoplasmic expression of hepatitis B core antigen (P = 0.028). No such differences were found in patients with and without precore mutations. Logistic regression showed that core promoter mutations were independently associated with cytoplasmic expression of hepatitis B core antigen (P = 0.026). Intrahepatic hepatitis B virus DNA levels correlated with serum hepatitis B virus DNA levels (r = 0.71, P < 0.001) and the percentage of hepatitis B core antigen-positive hepatocytes (r = 0.37, P = 0.047), but had no correlation with serum alanine aminotransferase levels nor the degree of inflammation and fibrosis. Conclusions: Patients with core promoter mutations had more severe inflammation and fibrosis, and more frequent cytoplasmic expression of hepatitis B core antigen. This suggested that core promoter mutations might cause more serious liver disease. © 2005 Blackwell Publishing Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/78174
ISSN
2015 Impact Factor: 6.32
2015 SCImago Journal Rankings: 2.833
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYuan, HJen_HK
dc.contributor.authorYuen, MFen_HK
dc.contributor.authorWong, DKHen_HK
dc.contributor.authorSum, SMen_HK
dc.contributor.authorSablon, Een_HK
dc.contributor.authorNg, IOLen_HK
dc.contributor.authorLai, CLen_HK
dc.date.accessioned2010-09-06T07:39:59Z-
dc.date.available2010-09-06T07:39:59Z-
dc.date.issued2005en_HK
dc.identifier.citationAlimentary Pharmacology And Therapeutics, 2005, v. 22 n. 4, p. 301-307en_HK
dc.identifier.issn0269-2813en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78174-
dc.description.abstractBackground: The details of liver histology of patients with precore and core promoter mutations are still not clear. Aim: To determine the role of precore and core promoter mutations in liver histology in Chinese patients with chronic hepatitis B. Patients and methods: Intrahepatic hepatitis B virus DNA (by COBAS Amplicor hepatitis B virus Monitor test) and precore and core promoter mutations (by a line probe assay) were measured in 54 chronic hepatitis B patients. Expression of hepatitis B core antigen, hepatitis B e antigen and hepatitis B surface antigen was determined by immunohistological staining. Histological activity index was scored according to Knodell's criteria. Results: Compared with patients without core promoter mutations, patients with core promoter mutations had more severe intrahepatic inflammation and fibrosis, and more cytoplasmic expression of hepatitis B core antigen (P = 0.028). No such differences were found in patients with and without precore mutations. Logistic regression showed that core promoter mutations were independently associated with cytoplasmic expression of hepatitis B core antigen (P = 0.026). Intrahepatic hepatitis B virus DNA levels correlated with serum hepatitis B virus DNA levels (r = 0.71, P < 0.001) and the percentage of hepatitis B core antigen-positive hepatocytes (r = 0.37, P = 0.047), but had no correlation with serum alanine aminotransferase levels nor the degree of inflammation and fibrosis. Conclusions: Patients with core promoter mutations had more severe inflammation and fibrosis, and more frequent cytoplasmic expression of hepatitis B core antigen. This suggested that core promoter mutations might cause more serious liver disease. © 2005 Blackwell Publishing Ltd.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/APTen_HK
dc.relation.ispartofAlimentary Pharmacology and Therapeuticsen_HK
dc.rightsAlimentary Pharmacology and Therapeutics. Copyright © Blackwell Publishing Ltd.en_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshDNA, Viral - geneticsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHepatitis B Core Antigens - metabolismen_HK
dc.subject.meshHepatitis B e Antigens - metabolismen_HK
dc.subject.meshHepatitis B, Chronic - genetics - metabolism - pathologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshMutation - geneticsen_HK
dc.subject.meshPromoter Regions, Genetic - geneticsen_HK
dc.titleImpact of precore and core promoter mutations on hepatic histology in patients with chronic hepatitis Ben_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0269-2813&volume=22&spage=301&epage=307&date=2005&atitle=Impact+of+Precore+and+Core+Promoter+Mutations+on+Hepatic+Histology+in+Patients+with+Chronic+Hepatitis+Ben_HK
dc.identifier.emailYuen, MF:mfyuen@hkucc.hku.hken_HK
dc.identifier.emailWong, DKH:danywong@hku.hken_HK
dc.identifier.emailNg, IOL:iolng@hkucc.hku.hken_HK
dc.identifier.emailLai, CL:hrmelcl@hku.hken_HK
dc.identifier.authorityYuen, MF=rp00479en_HK
dc.identifier.authorityWong, DKH=rp00492en_HK
dc.identifier.authorityNg, IOL=rp00335en_HK
dc.identifier.authorityLai, CL=rp00314en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1365-2036.2005.02563.xen_HK
dc.identifier.pmid16097996-
dc.identifier.scopuseid_2-s2.0-23944462343en_HK
dc.identifier.hkuros115277en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-23944462343&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume22en_HK
dc.identifier.issue4en_HK
dc.identifier.spage301en_HK
dc.identifier.epage307en_HK
dc.identifier.isiWOS:000231148500004-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridYuan, HJ=7402446707en_HK
dc.identifier.scopusauthoridYuen, MF=7102031955en_HK
dc.identifier.scopusauthoridWong, DKH=7401535819en_HK
dc.identifier.scopusauthoridSum, SM=6603889132en_HK
dc.identifier.scopusauthoridSablon, E=6603694538en_HK
dc.identifier.scopusauthoridNg, IOL=7102753722en_HK
dc.identifier.scopusauthoridLai, CL=7403086396en_HK
dc.identifier.citeulike278697-

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