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Article: Occult hepatitis B infection and HBV replicative activity in patients with cryptogenic cause of hepatocellular carcinoma

TitleOccult hepatitis B infection and HBV replicative activity in patients with cryptogenic cause of hepatocellular carcinoma
Authors
Issue Date2011
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
Citation
Hepatology, 2011, v. 54 n. 3, p. 829-836 How to Cite?
AbstractWe aimed to investigate the incidence of occult hepatitis B infection (OBI) in patients with "cryptogenic" hepatocellular carcinoma (HCC) and to study the HBV replicative activity in these patients. Tumorous and adjacent nontumorous liver tissues were obtained from 33 cryptogenic HCC patients and 28 HCC patients with identifiable causes (13 with chronic hepatitis B [CHB], six with chronic hepatitis C, and nine alcohol-related). OBI was identified by nested polymerase chain reaction (PCR). Intrahepatic HBV DNA, covalently closed circular DNA (cccDNA), and pregenomic RNA (pgRNA) were quantified by real-time PCR and reverse-transcription PCR (RT-PCR), respectively. OBI was identified in 24 (73%) cryptogenic HCC patients, one (17%) HCC patient with HCV, and five (56%) patients with alcohol-related HCC. In HCC patients with OBI, HBV DNA were detected in ≥2 HBV genomic regions more often in nontumorous tissues than in tumorous tissues (90% versus 57%, respectively; P = 0.007). Cryptogenic HCC patients with OBI had lower intrahepatic total HBV DNA levels than HCC patients with CHB (median: 0.010 versus 3.19 copies/cell, respectively; P < 0.0001). Only six (26%) cryptogenic HCC patients with OBI had detectable cccDNA (median: <0.0002 copies/cell), which was significantly lower than that of the CHB patients (median: 0.005 copies/cell; P < 0.0001). HBV pgRNA were detectable in 12 (52%) cryptogenic HCC patients with OBI (median: 0.0001 copies/cell), which was significantly lower than that of the CHB patients (median: 2.90 copies/cell; P < 0.001). Conclusion: 73% of patients with apparently unidentifiable causes for HCC were HBV-related. The detection rate was higher in nontumorous tissues than tumorous tissues. The low intrahepatic HBV DNA and pgRNA levels indicated that persistent viral replication and possibly HBV integration are the likely causes of HCC in OBI patients. © 2011 American Association for the Study of Liver Diseases.
Persistent Identifierhttp://hdl.handle.net/10722/139749
ISSN
2015 Impact Factor: 11.711
2015 SCImago Journal Rankings: 4.752
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, DKHen_HK
dc.contributor.authorHuang, FYen_HK
dc.contributor.authorLai, CLen_HK
dc.contributor.authorPoon, RTPen_HK
dc.contributor.authorSeto, WKen_HK
dc.contributor.authorFung, Jen_HK
dc.contributor.authorHung, IFNen_HK
dc.contributor.authorYuen, MFen_HK
dc.date.accessioned2011-09-23T05:55:13Z-
dc.date.available2011-09-23T05:55:13Z-
dc.date.issued2011en_HK
dc.identifier.citationHepatology, 2011, v. 54 n. 3, p. 829-836en_HK
dc.identifier.issn0270-9139en_HK
dc.identifier.urihttp://hdl.handle.net/10722/139749-
dc.description.abstractWe aimed to investigate the incidence of occult hepatitis B infection (OBI) in patients with "cryptogenic" hepatocellular carcinoma (HCC) and to study the HBV replicative activity in these patients. Tumorous and adjacent nontumorous liver tissues were obtained from 33 cryptogenic HCC patients and 28 HCC patients with identifiable causes (13 with chronic hepatitis B [CHB], six with chronic hepatitis C, and nine alcohol-related). OBI was identified by nested polymerase chain reaction (PCR). Intrahepatic HBV DNA, covalently closed circular DNA (cccDNA), and pregenomic RNA (pgRNA) were quantified by real-time PCR and reverse-transcription PCR (RT-PCR), respectively. OBI was identified in 24 (73%) cryptogenic HCC patients, one (17%) HCC patient with HCV, and five (56%) patients with alcohol-related HCC. In HCC patients with OBI, HBV DNA were detected in ≥2 HBV genomic regions more often in nontumorous tissues than in tumorous tissues (90% versus 57%, respectively; P = 0.007). Cryptogenic HCC patients with OBI had lower intrahepatic total HBV DNA levels than HCC patients with CHB (median: 0.010 versus 3.19 copies/cell, respectively; P < 0.0001). Only six (26%) cryptogenic HCC patients with OBI had detectable cccDNA (median: <0.0002 copies/cell), which was significantly lower than that of the CHB patients (median: 0.005 copies/cell; P < 0.0001). HBV pgRNA were detectable in 12 (52%) cryptogenic HCC patients with OBI (median: 0.0001 copies/cell), which was significantly lower than that of the CHB patients (median: 2.90 copies/cell; P < 0.001). Conclusion: 73% of patients with apparently unidentifiable causes for HCC were HBV-related. The detection rate was higher in nontumorous tissues than tumorous tissues. The low intrahepatic HBV DNA and pgRNA levels indicated that persistent viral replication and possibly HBV integration are the likely causes of HCC in OBI patients. © 2011 American Association for the Study of Liver Diseases.en_HK
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/en_HK
dc.relation.ispartofHepatologyen_HK
dc.rightsHepatology. Copyright © John Wiley & Sons, Inc.-
dc.subject.meshCarcinoma, Hepatocellular - virology-
dc.subject.meshHepatitis B virus - physiology-
dc.subject.meshHepatitis B, Chronic - complications-
dc.subject.meshLiver Neoplasms - virology-
dc.subject.meshVirus Replication-
dc.titleOccult hepatitis B infection and HBV replicative activity in patients with cryptogenic cause of hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.emailWong, DKH: danywong@hku.hken_HK
dc.identifier.emailLai, CL: hrmelcl@hku.hken_HK
dc.identifier.emailPoon, RTP: poontp@hku.hken_HK
dc.identifier.emailSeto, WK: wkseto2@hku.hken_HK
dc.identifier.emailFung, J: jfung@sicklehut.comen_HK
dc.identifier.emailHung, IFN: ivanhung@hkucc.hku.hken_HK
dc.identifier.emailYuen, MF: mfyuen@hku.hken_HK
dc.identifier.authorityWong, DKH=rp00492en_HK
dc.identifier.authorityLai, CL=rp00314en_HK
dc.identifier.authorityPoon, RTP=rp00446en_HK
dc.identifier.authoritySeto, WK=rp01659en_HK
dc.identifier.authorityFung, J=rp00518en_HK
dc.identifier.authorityHung, IFN=rp00508en_HK
dc.identifier.authorityYuen, MF=rp00479en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/hep.24551en_HK
dc.identifier.pmid21809355-
dc.identifier.scopuseid_2-s2.0-80051979890en_HK
dc.identifier.hkuros192500en_US
dc.identifier.hkuros213691-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80051979890&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume54en_HK
dc.identifier.issue3en_HK
dc.identifier.spage829en_HK
dc.identifier.epage836en_HK
dc.identifier.eissn1527-3350-
dc.identifier.isiWOS:000294738300011-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, DKH=7401535819en_HK
dc.identifier.scopusauthoridHuang, FY=8644138400en_HK
dc.identifier.scopusauthoridLai, CL=7403086396en_HK
dc.identifier.scopusauthoridPoon, RTP=7103097223en_HK
dc.identifier.scopusauthoridSeto, WK=23390675900en_HK
dc.identifier.scopusauthoridFung, J=23091109300en_HK
dc.identifier.scopusauthoridHung, IFN=7006103457en_HK
dc.identifier.scopusauthoridYuen, MF=7102031955en_HK

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