File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Kinetics and Risk of De Novo Hepatitis B Infection in HBsAg-Negative Patients Undergoing Cytotoxic Chemotherapy

TitleKinetics and Risk of De Novo Hepatitis B Infection in HBsAg-Negative Patients Undergoing Cytotoxic Chemotherapy
Authors
Issue Date2006
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastro
Citation
Gastroenterology, 2006, v. 131 n. 1, p. 59-68 How to Cite?
AbstractBackground & Aims: De novo hepatitis B virus (HBV)-related hepatitis after chemotherapy results in high morbidity and mortality. We evaluate the clinical course of de novo HBV-related hepatitis after chemotherapy. Methods: Two hundred forty-four consecutive hepatitis B surface antigen (HBsAg)-negative lymphoma patients treated with chemotherapy were followed up for a median of 12.4 (range, 0.1-65.0) months. Serially collected serum samples were analyzed for hepatitis, serum HBV DNA, and HBsAg seroreversion. Results: Eight of the 244 patients (3.3%) developed de novo HBV-related hepatitis. A 100-fold increase in serum HBV DNA preceded de novo HBV-related hepatitis by a median of 18.5 (range, 12-28) weeks. All 8 patients had normal serum alanine aminotransaminase level when the 100-fold increase in serum HBV DNA occurred. Patients with de novo HBV-related hepatitis were more likely to have occult HBV infection before chemotherapy. Direct sequencing results showed that these 8 patients had de novo HBV-related hepatitis from reactivation of occult HBV infection. Three of the 8 patients with de novo HBV-related hepatitis compared with 6 of the 236 patients without de novo HBV-related hepatitis developed fulminant hepatic failure (37.5% vs 2.5%, respectively, P < .001). On multivariate Cox analysis, de novo HBV-related hepatitis was independently associated with a higher risk of fulminant hepatic failure (relative risk, 29.854; 95% confidence interval: 4.844-183.980; P < .001). Conclusions: Close surveillance for a 100-fold increase in HBV DNA is recommended for HBsAg-negative patients treated with chemotherapy so that early commencement of antiviral therapy can be initiated before the occurrence of de novo HBV-related hepatitis. © 2006 American Gastroenterological Association Institute.
Persistent Identifierhttp://hdl.handle.net/10722/162992
ISSN
2015 Impact Factor: 18.187
2015 SCImago Journal Rankings: 7.170
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHui, CKen_US
dc.contributor.authorCheung, WWWen_US
dc.contributor.authorZhang, HYen_US
dc.contributor.authorAu, WYen_US
dc.contributor.authorYueng, YHen_US
dc.contributor.authorLeung, AYHen_US
dc.contributor.authorLeung, Nen_US
dc.contributor.authorLuk, JMen_US
dc.contributor.authorLie, AKWen_US
dc.contributor.authorKwong, YLen_US
dc.contributor.authorLiang, Ren_US
dc.contributor.authorLau, GKKen_US
dc.date.accessioned2012-09-05T05:26:20Z-
dc.date.available2012-09-05T05:26:20Z-
dc.date.issued2006en_US
dc.identifier.citationGastroenterology, 2006, v. 131 n. 1, p. 59-68en_US
dc.identifier.issn0016-5085en_US
dc.identifier.urihttp://hdl.handle.net/10722/162992-
dc.description.abstractBackground & Aims: De novo hepatitis B virus (HBV)-related hepatitis after chemotherapy results in high morbidity and mortality. We evaluate the clinical course of de novo HBV-related hepatitis after chemotherapy. Methods: Two hundred forty-four consecutive hepatitis B surface antigen (HBsAg)-negative lymphoma patients treated with chemotherapy were followed up for a median of 12.4 (range, 0.1-65.0) months. Serially collected serum samples were analyzed for hepatitis, serum HBV DNA, and HBsAg seroreversion. Results: Eight of the 244 patients (3.3%) developed de novo HBV-related hepatitis. A 100-fold increase in serum HBV DNA preceded de novo HBV-related hepatitis by a median of 18.5 (range, 12-28) weeks. All 8 patients had normal serum alanine aminotransaminase level when the 100-fold increase in serum HBV DNA occurred. Patients with de novo HBV-related hepatitis were more likely to have occult HBV infection before chemotherapy. Direct sequencing results showed that these 8 patients had de novo HBV-related hepatitis from reactivation of occult HBV infection. Three of the 8 patients with de novo HBV-related hepatitis compared with 6 of the 236 patients without de novo HBV-related hepatitis developed fulminant hepatic failure (37.5% vs 2.5%, respectively, P < .001). On multivariate Cox analysis, de novo HBV-related hepatitis was independently associated with a higher risk of fulminant hepatic failure (relative risk, 29.854; 95% confidence interval: 4.844-183.980; P < .001). Conclusions: Close surveillance for a 100-fold increase in HBV DNA is recommended for HBsAg-negative patients treated with chemotherapy so that early commencement of antiviral therapy can be initiated before the occurrence of de novo HBV-related hepatitis. © 2006 American Gastroenterological Association Institute.en_US
dc.languageengen_US
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastroen_US
dc.relation.ispartofGastroenterologyen_US
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshAged, 80 And Overen_US
dc.subject.meshAntiviral Agents - Therapeutic Useen_US
dc.subject.meshDna, Viral - Analysisen_US
dc.subject.meshDisease Progressionen_US
dc.subject.meshFemaleen_US
dc.subject.meshFollow-Up Studiesen_US
dc.subject.meshHepatitis B - Complications - Drug Therapy - Virologyen_US
dc.subject.meshHepatitis B Surface Antigens - Immunologyen_US
dc.subject.meshHepatitis B Virus - Genetics - Immunologyen_US
dc.subject.meshHumansen_US
dc.subject.meshLiver Failure, Acute - Epidemiology - Etiologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPrevalenceen_US
dc.subject.meshPrognosisen_US
dc.subject.meshRetrospective Studiesen_US
dc.subject.meshRisk Factorsen_US
dc.titleKinetics and Risk of De Novo Hepatitis B Infection in HBsAg-Negative Patients Undergoing Cytotoxic Chemotherapyen_US
dc.typeArticleen_US
dc.identifier.emailLeung, AYH:ayhleung@hku.hken_US
dc.identifier.emailLuk, JM:jmluk@hkucc.hku.hken_US
dc.identifier.emailKwong, Y:ylkwong@hku.hken_US
dc.identifier.emailLiang, R:rliang@hku.hken_US
dc.identifier.authorityLeung, AYH=rp00265en_US
dc.identifier.authorityLuk, JM=rp00349en_US
dc.identifier.authorityKwong, Y=rp00358en_US
dc.identifier.authorityLiang, R=rp00345en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1053/j.gastro.2006.04.015en_US
dc.identifier.pmid16831590-
dc.identifier.scopuseid_2-s2.0-33745753570en_US
dc.identifier.hkuros120529-
dc.identifier.hkuros119655-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33745753570&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume131en_US
dc.identifier.issue1en_US
dc.identifier.spage59en_US
dc.identifier.epage68en_US
dc.identifier.isiWOS:000238983300015-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridHui, C=35082057900en_US
dc.identifier.scopusauthoridCheung, WWW=8615134400en_US
dc.identifier.scopusauthoridZhang, H=8965962000en_US
dc.identifier.scopusauthoridAu, W=7202383089en_US
dc.identifier.scopusauthoridYueng, Y=8965962100en_US
dc.identifier.scopusauthoridLeung, AYH=7403012668en_US
dc.identifier.scopusauthoridLeung, N=26643107200en_US
dc.identifier.scopusauthoridLuk, JM=7006777791en_US
dc.identifier.scopusauthoridLie, AKW=7004510870en_US
dc.identifier.scopusauthoridKwong, Y=7102818954en_US
dc.identifier.scopusauthoridLiang, R=26643224900en_US
dc.identifier.scopusauthoridLau, GKK=7102301257en_US
dc.identifier.citeulike5402014-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats