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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
Title | The role of hepatitis B core-related antigen in predicting HBV reactivation among HBsAg-negative, anti-HBc-positive individuals undergoing immunosuppressive therapy |
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Authors | |
Keywords | Medical sciences Gastroenterology |
Issue Date | 2015 |
Publisher | John 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? |
Abstract | BACKGROUND: 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. |
Description | Poster 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 Identifier | http://hdl.handle.net/10722/226491 |
ISSN | 2023 Impact Factor: 12.9 2023 SCImago Journal Rankings: 5.011 |
DC Field | Value | Language |
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dc.contributor.author | Seto, WK | - |
dc.contributor.author | Wong, D | - |
dc.contributor.author | Liu, SHK | - |
dc.contributor.author | Fung, J | - |
dc.contributor.author | Lai, CL | - |
dc.contributor.author | Yuen, MF | - |
dc.date.accessioned | 2016-06-17T07:44:29Z | - |
dc.date.available | 2016-06-17T07:44:29Z | - |
dc.date.issued | 2015 | - |
dc.identifier.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 | - |
dc.identifier.issn | 0270-9139 | - |
dc.identifier.uri | http://hdl.handle.net/10722/226491 | - |
dc.description | Poster Session 3 - Hepatitis B: Epidemiology and Natural History: no. 1550 | - |
dc.description | 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 | - |
dc.description.abstract | BACKGROUND: 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.language | eng | - |
dc.publisher | John Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/ | - |
dc.relation.ispartof | Hepatology | - |
dc.rights | Hepatology. Copyright © John Wiley & Sons, Inc. | - |
dc.subject | Medical sciences | - |
dc.subject | Gastroenterology | - |
dc.title | The role of hepatitis B core-related antigen in predicting HBV reactivation among HBsAg-negative, anti-HBc-positive individuals undergoing immunosuppressive therapy | - |
dc.type | Conference_Paper | - |
dc.identifier.email | Seto, WK: wkseto@hku.hk | - |
dc.identifier.email | Wong, D: danywong@hku.hk | - |
dc.identifier.email | Liu, SHK: drkliu@hku.hk | - |
dc.identifier.email | Fung, J: jfung@hkucc.hku.hk | - |
dc.identifier.email | Lai, CL: hrmelcl@hkucc.hku.hk | - |
dc.identifier.email | Yuen, MF: mfyuen@hku.hk | - |
dc.identifier.authority | Seto, WK=rp01659 | - |
dc.identifier.authority | Wong, D=rp00492 | - |
dc.identifier.authority | Fung, J=rp00518 | - |
dc.identifier.authority | Lai, CL=rp00314 | - |
dc.identifier.authority | Yuen, MF=rp00479 | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1002/hep.28233 | - |
dc.identifier.hkuros | 258656 | - |
dc.identifier.volume | 62 | - |
dc.identifier.issue | suppl. S1 | - |
dc.identifier.spage | 966A, abstarct no. 1550 | - |
dc.identifier.epage | 966A, abstarct no. 1550 | - |
dc.publisher.place | United States | - |
dc.identifier.issnl | 0270-9139 | - |