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Conference Paper: The role of hepatitis B core-related antigen in predicting HBV reactivation among HBsAg-negative, anti-HBc-positive individuals undergoing immunosuppressive therapy

TitleThe role of hepatitis B core-related antigen in predicting HBV reactivation among HBsAg-negative, anti-HBc-positive individuals undergoing immunosuppressive therapy
Authors
KeywordsMedical sciences
Gastroenterology
Issue Date2015
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
Citation
The 66th Annual Meeting of the American Association for the Study of Liver Diseases (AASLD Liver Meeting 2015), San Francisco, CA., 13-17 November 2015. In Hepatology, 2015, v. 62 suppl. S1, p. 966A, abstarct no. 1550 How to Cite?
AbstractBACKGROUND: Hepatitis B core-related antigen (HBcrAg) detects an identical amino-acid sequence shared by hepatitis B e antigen, hepatitis B core antigen and 22kDa precore protein. Serum HBcrAg correlates with disease activity of chronic hepatitis B (CHB), and can be detected in a considerable proportion of CHB patients after hepatitis B surface antigen (HBsAg) seroclearance. Its role in predicting HBV reactivation among HBsAg-negative, antibody to hepatitis B core antigen (anti-HBc) positive has not been explored. METHODS: We retrieved stored plasma samples of HBsAg-negative, anti-HBc positive, patients with undetectable HBV DNA at baseline who were enrolled into two prospective studies, which aimed at investigating the rate of HBV reactivation during rituximab-containing chemotherapy and hematopoietic stem-cell transplantation (HSCT) (ClinicalTrials. gov identifier NCT01502397 and NCT01481647 respectively). HBV reactivation was defined as detectable HBV DNA (≥10 IU/mL). Serum HBcrAg (lower limit of detection 100 U/mL) was measured using a chemiluminscent enzyme immunoassay (Fujirebio Inc, Tokyo, Japan) at baseline and at every 3 months up to the date of last follow-up. RESULTS: We included 131 HBsAg-negative, anti-HBc positive patients (rituximab/HSCT 47.3%/52.7%), with a mean age of 57.4 (±15.1) years and a mean follow-up duration of 53.3 (±35.0) weeks. 32 patients developed HBV reactivation (rituximab/HSCT 56.3%/43.7%); the 2-year cumulative rate of HBV reactivation was 39.2%. 21 patients (16.0%) and 25 patients (19.1%) had detectable serum HBcrAg at either baseline or any time point before reactivation respectively. The median detectable baseline HBcrAg level was 400 (range 200-5,300) U/mL. Baseline serum HBcrAg positivity, compared to baseline HBcrAg-negative patients, had a significantly higher 2-year cumulative rate of HBV reactivation (75.8% versus 29.9% respectively, p<0.001). When comparing HBcrAg-positivity at any time point before reactivation versus persistent HBcrAg-negativity, the difference was even greater (83.6% versus 23.2% respectively, p<0.001). Baseline HBcrAg-positivity was independently associated with HBV reactivation via multivariate Cox regression for both rituximab (n=62) (p=0.003, OR 4.9, 95% CI 1.7-13.9) and HSCT (n=69) (p=0.012, HR 4.8, 95% CI 1.4-16.1). The association of HBcrAg-positivity with HBV reactivation among rituximab patients was stronger than that of anti-HBs negativity (p=0.050, OR 2.6, 95% CI 1.0-6.8). CONCLUSION: Serum HBcrAg could potentially play a role in identifying HBsAg-negative, anti-HBc positive patients who would best benefit from prophylactic nucleoside analogue therapy.
DescriptionPoster Session 3 - Hepatitis B: Epidemiology and Natural History: no. 1550
This FREE journal suppl. entitled: Special Issue: The 66th Annual Meeting of the American Association for the Study of Liver Diseases: The Liver Meeting 2015
Persistent Identifierhttp://hdl.handle.net/10722/226491
ISSN
2015 Impact Factor: 11.711
2015 SCImago Journal Rankings: 4.752

 

DC FieldValueLanguage
dc.contributor.authorSeto, WK-
dc.contributor.authorWong, D-
dc.contributor.authorLiu, SHK-
dc.contributor.authorFung, J-
dc.contributor.authorLai, CL-
dc.contributor.authorYuen, MF-
dc.date.accessioned2016-06-17T07:44:29Z-
dc.date.available2016-06-17T07:44:29Z-
dc.date.issued2015-
dc.identifier.citationThe 66th Annual Meeting of the American Association for the Study of Liver Diseases (AASLD Liver Meeting 2015), San Francisco, CA., 13-17 November 2015. In Hepatology, 2015, v. 62 suppl. S1, p. 966A, abstarct no. 1550-
dc.identifier.issn0270-9139-
dc.identifier.urihttp://hdl.handle.net/10722/226491-
dc.descriptionPoster Session 3 - Hepatitis B: Epidemiology and Natural History: no. 1550-
dc.descriptionThis FREE journal suppl. entitled: Special Issue: The 66th Annual Meeting of the American Association for the Study of Liver Diseases: The Liver Meeting 2015-
dc.description.abstractBACKGROUND: Hepatitis B core-related antigen (HBcrAg) detects an identical amino-acid sequence shared by hepatitis B e antigen, hepatitis B core antigen and 22kDa precore protein. Serum HBcrAg correlates with disease activity of chronic hepatitis B (CHB), and can be detected in a considerable proportion of CHB patients after hepatitis B surface antigen (HBsAg) seroclearance. Its role in predicting HBV reactivation among HBsAg-negative, antibody to hepatitis B core antigen (anti-HBc) positive has not been explored. METHODS: We retrieved stored plasma samples of HBsAg-negative, anti-HBc positive, patients with undetectable HBV DNA at baseline who were enrolled into two prospective studies, which aimed at investigating the rate of HBV reactivation during rituximab-containing chemotherapy and hematopoietic stem-cell transplantation (HSCT) (ClinicalTrials. gov identifier NCT01502397 and NCT01481647 respectively). HBV reactivation was defined as detectable HBV DNA (≥10 IU/mL). Serum HBcrAg (lower limit of detection 100 U/mL) was measured using a chemiluminscent enzyme immunoassay (Fujirebio Inc, Tokyo, Japan) at baseline and at every 3 months up to the date of last follow-up. RESULTS: We included 131 HBsAg-negative, anti-HBc positive patients (rituximab/HSCT 47.3%/52.7%), with a mean age of 57.4 (±15.1) years and a mean follow-up duration of 53.3 (±35.0) weeks. 32 patients developed HBV reactivation (rituximab/HSCT 56.3%/43.7%); the 2-year cumulative rate of HBV reactivation was 39.2%. 21 patients (16.0%) and 25 patients (19.1%) had detectable serum HBcrAg at either baseline or any time point before reactivation respectively. The median detectable baseline HBcrAg level was 400 (range 200-5,300) U/mL. Baseline serum HBcrAg positivity, compared to baseline HBcrAg-negative patients, had a significantly higher 2-year cumulative rate of HBV reactivation (75.8% versus 29.9% respectively, p<0.001). When comparing HBcrAg-positivity at any time point before reactivation versus persistent HBcrAg-negativity, the difference was even greater (83.6% versus 23.2% respectively, p<0.001). Baseline HBcrAg-positivity was independently associated with HBV reactivation via multivariate Cox regression for both rituximab (n=62) (p=0.003, OR 4.9, 95% CI 1.7-13.9) and HSCT (n=69) (p=0.012, HR 4.8, 95% CI 1.4-16.1). The association of HBcrAg-positivity with HBV reactivation among rituximab patients was stronger than that of anti-HBs negativity (p=0.050, OR 2.6, 95% CI 1.0-6.8). CONCLUSION: Serum HBcrAg could potentially play a role in identifying HBsAg-negative, anti-HBc positive patients who would best benefit from prophylactic nucleoside analogue therapy.-
dc.languageeng-
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/-
dc.relation.ispartofHepatology-
dc.rightsHepatology. Copyright © John Wiley & Sons, Inc.-
dc.subjectMedical sciences-
dc.subjectGastroenterology-
dc.titleThe role of hepatitis B core-related antigen in predicting HBV reactivation among HBsAg-negative, anti-HBc-positive individuals undergoing immunosuppressive therapy-
dc.typeConference_Paper-
dc.identifier.emailSeto, WK: wkseto@hku.hk-
dc.identifier.emailWong, D: danywong@hku.hk-
dc.identifier.emailLiu, SHK: drkliu@hku.hk-
dc.identifier.emailFung, J: jfung@hkucc.hku.hk-
dc.identifier.emailLai, CL: hrmelcl@hkucc.hku.hk-
dc.identifier.emailYuen, MF: mfyuen@hku.hk-
dc.identifier.authoritySeto, WK=rp01659-
dc.identifier.authorityWong, D=rp00492-
dc.identifier.authorityFung, J=rp00518-
dc.identifier.authorityLai, CL=rp00314-
dc.identifier.authorityYuen, MF=rp00479-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/hep.28233-
dc.identifier.hkuros258656-
dc.identifier.volume62-
dc.identifier.issuesuppl. S1-
dc.identifier.spage966A, abstarct no. 1550-
dc.identifier.epage966A, abstarct no. 1550-
dc.publisher.placeUnited States-

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