File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: T1653 mutation in the box α increases the risk of hepatocellular carcinoma in patients with chronic hepatitis B virus genotype C Infection

TitleT1653 mutation in the box α increases the risk of hepatocellular carcinoma in patients with chronic hepatitis B virus genotype C Infection
Authors
Issue Date2006
PublisherOxford University Press. The Journal's web site is located at http://www.oxfordjournals.org/our_journals/cid/
Citation
Clinical Infectious Diseases, 2006, v. 42 n. 1, p. 1-7 How to Cite?
AbstractBackground. Most patients with chronic hepatitis B virus infection become carriers of inactive virus after hepatitis B e antigen seroconversion; however, a subgroup of patients have persistent abnormal transaminase levels and develop hepatocellular carcinoma after seroconversion. Methods. In an age-matched case-control study, 40 carriers of inactive virus (mean age ± standard deviation [SD], 50.9 ± 11.1 years), 40 parents with chronic hepatitis (mean age ± SD, 50.2 ± 8.9 years), and 40 patients with hepatocellular carcinoma (mean age ± SD, 50.7 ± 9.4 years) who were infected with hepatitis B virus genotype C and had test results positive for antibody to hepatitis B e antigen were analyzed. Results. The prevalence of T1653 in the box α was significantly higher among patients with hepatocellular carcinoma than among carriers|of inactive virus who did not have hepatocellular carcinoma (70% vs. 25%; P < .0001) or chronic hepatitis (70% vs. 35%; P = .003). Mutations in the basic core promoter region (T1762/A1764) were frequently found in all groups, regardless of clinical status (in 77.5% of carriers of inactive virus, 77.5% of patients with chronic hepatitis, and 90% of patients with hepatocellular carcinoma). In the multivariate analysis, the presence of T1653, an alanine aminotransferase level of ≥ 37 U/L, and a platelet count of < 18 × 104 platelets/ mm3 were independent predictive values for hepatocellular carcinoma (odds ratio [95% confidence interval], 5.05 [1.56-16.35], 12.56 [3.05-51.77], and 11.5 [3.47-38.21], respectively). High α-fetoprotein level was the only independent predictive value for T1653 in patients with hepatocellular carcinoma (odds ratio, 12.67; 95% confidence interval, 1.19-134.17]). Among patients with test results positive for antibody to hepatitis B e antigen who had hepatocellular carcinoma and were infected with different genotypes of hepatitis B virus, the prevalence of T1653 was 40%, 15%, 25%, 25%, 67%, and 23% in patients infected with hepatitis B virus genotypes Aa, Ae, Ba, Bj, C, and D, respectively (P < .05 for genotype C vs. genotypes Ae, Ba, Bj, or D). Conclusions. Our data indicate that the addition of T1653 mutation in the box a to the basic core promoter mutation increases the risk of hepatocellular carcinoma in patients with hepatitis B virus genotype C. © 2005 by the Infectious Diseases Society of America. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/162909
ISSN
2015 Impact Factor: 8.736
2015 SCImago Journal Rankings: 4.742
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorIto, Ken_US
dc.contributor.authorTanaka, Yen_US
dc.contributor.authorOrito, Een_US
dc.contributor.authorSugiyama, Men_US
dc.contributor.authorFujiwara, Ken_US
dc.contributor.authorSugauchi, Fen_US
dc.contributor.authorKato, Ten_US
dc.contributor.authorTokita, Hen_US
dc.contributor.authorIzumi, Nen_US
dc.contributor.authorKato, Men_US
dc.contributor.authorYuen, MFen_US
dc.contributor.authorLai, CLen_US
dc.contributor.authorGish, RGen_US
dc.contributor.authorUeda, Ren_US
dc.contributor.authorMizokemi, Men_US
dc.date.accessioned2012-09-05T05:25:09Z-
dc.date.available2012-09-05T05:25:09Z-
dc.date.issued2006en_US
dc.identifier.citationClinical Infectious Diseases, 2006, v. 42 n. 1, p. 1-7en_US
dc.identifier.issn1058-4838en_US
dc.identifier.urihttp://hdl.handle.net/10722/162909-
dc.description.abstractBackground. Most patients with chronic hepatitis B virus infection become carriers of inactive virus after hepatitis B e antigen seroconversion; however, a subgroup of patients have persistent abnormal transaminase levels and develop hepatocellular carcinoma after seroconversion. Methods. In an age-matched case-control study, 40 carriers of inactive virus (mean age ± standard deviation [SD], 50.9 ± 11.1 years), 40 parents with chronic hepatitis (mean age ± SD, 50.2 ± 8.9 years), and 40 patients with hepatocellular carcinoma (mean age ± SD, 50.7 ± 9.4 years) who were infected with hepatitis B virus genotype C and had test results positive for antibody to hepatitis B e antigen were analyzed. Results. The prevalence of T1653 in the box α was significantly higher among patients with hepatocellular carcinoma than among carriers|of inactive virus who did not have hepatocellular carcinoma (70% vs. 25%; P < .0001) or chronic hepatitis (70% vs. 35%; P = .003). Mutations in the basic core promoter region (T1762/A1764) were frequently found in all groups, regardless of clinical status (in 77.5% of carriers of inactive virus, 77.5% of patients with chronic hepatitis, and 90% of patients with hepatocellular carcinoma). In the multivariate analysis, the presence of T1653, an alanine aminotransferase level of ≥ 37 U/L, and a platelet count of < 18 × 104 platelets/ mm3 were independent predictive values for hepatocellular carcinoma (odds ratio [95% confidence interval], 5.05 [1.56-16.35], 12.56 [3.05-51.77], and 11.5 [3.47-38.21], respectively). High α-fetoprotein level was the only independent predictive value for T1653 in patients with hepatocellular carcinoma (odds ratio, 12.67; 95% confidence interval, 1.19-134.17]). Among patients with test results positive for antibody to hepatitis B e antigen who had hepatocellular carcinoma and were infected with different genotypes of hepatitis B virus, the prevalence of T1653 was 40%, 15%, 25%, 25%, 67%, and 23% in patients infected with hepatitis B virus genotypes Aa, Ae, Ba, Bj, C, and D, respectively (P < .05 for genotype C vs. genotypes Ae, Ba, Bj, or D). Conclusions. Our data indicate that the addition of T1653 mutation in the box a to the basic core promoter mutation increases the risk of hepatocellular carcinoma in patients with hepatitis B virus genotype C. © 2005 by the Infectious Diseases Society of America. All rights reserved.en_US
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://www.oxfordjournals.org/our_journals/cid/en_US
dc.relation.ispartofClinical Infectious Diseasesen_US
dc.subject.meshCarcinoma, Hepatocellular - Etiology - Geneticsen_US
dc.subject.meshCase-Control Studiesen_US
dc.subject.meshFemaleen_US
dc.subject.meshGenotypeen_US
dc.subject.meshHepatitis B Virus - Classification - Geneticsen_US
dc.subject.meshHepatitis B, Chronic - Complicationsen_US
dc.subject.meshHumansen_US
dc.subject.meshLiver Neoplasms - Etiology - Geneticsen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshMutationen_US
dc.subject.meshRisk Factorsen_US
dc.titleT1653 mutation in the box α increases the risk of hepatocellular carcinoma in patients with chronic hepatitis B virus genotype C Infectionen_US
dc.typeArticleen_US
dc.identifier.emailYuen, MF:mfyuen@hkucc.hku.hken_US
dc.identifier.emailLai, CL:hrmelcl@hku.hken_US
dc.identifier.authorityYuen, MF=rp00479en_US
dc.identifier.authorityLai, CL=rp00314en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1086/498522en_US
dc.identifier.pmid16323084en_US
dc.identifier.scopuseid_2-s2.0-29244449650en_US
dc.identifier.hkuros115273-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-29244449650&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume42en_US
dc.identifier.issue1en_US
dc.identifier.spage1en_US
dc.identifier.epage7en_US
dc.identifier.isiWOS:000233698900007-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridIto, K=9242748800en_US
dc.identifier.scopusauthoridTanaka, Y=7405315865en_US
dc.identifier.scopusauthoridOrito, E=7006161634en_US
dc.identifier.scopusauthoridSugiyama, M=8108431700en_US
dc.identifier.scopusauthoridFujiwara, K=7403468620en_US
dc.identifier.scopusauthoridSugauchi, F=7004837927en_US
dc.identifier.scopusauthoridKato, T=7405277868en_US
dc.identifier.scopusauthoridTokita, H=7006437893en_US
dc.identifier.scopusauthoridIzumi, N=7102192003en_US
dc.identifier.scopusauthoridKato, M=7406302992en_US
dc.identifier.scopusauthoridYuen, MF=7102031955en_US
dc.identifier.scopusauthoridLai, CL=7403086396en_US
dc.identifier.scopusauthoridGish, RG=7007037133en_US
dc.identifier.scopusauthoridUeda, R=35376281000en_US
dc.identifier.scopusauthoridMizokemi, M=10143788100en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats