Two distinct subtypes of hepatitis B virus-related acute liver failure are separable by quantitative serum immunoglobulin M anti-hepatitis B core antibody and hepatitis B virus DNA levels
Hepatitis B virus (HBV)‐related acute liver failure (HBV‐ALF) may occur after acute HBV infection (AHBV‐ALF) or during an exacerbation of chronic HBV infection (CHBV‐ALF). Clinical differentiation of the two is often difficult if a previous history of HBV is not available. Quantitative measurements...
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| Published in | Hepatology (Baltimore, Md.) Vol. 55; no. 3; pp. 676 - 684 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Hoboken
Wiley Subscription Services, Inc., A Wiley Company
01.03.2012
Wiley Wiley Subscription Services, Inc |
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| Abstract | Hepatitis B virus (HBV)‐related acute liver failure (HBV‐ALF) may occur after acute HBV infection (AHBV‐ALF) or during an exacerbation of chronic HBV infection (CHBV‐ALF). Clinical differentiation of the two is often difficult if a previous history of HBV is not available. Quantitative measurements of immunoglobulin M (IgM) anti–hepatitis B core antibody (anti‐HBc) titers and of HBV viral loads (VLs) might allow the separation of AHBV‐ALF from CHBV‐ALF. Of 1,602 patients with ALF, 60 met clinical criteria for AHBV‐ALF and 27 for CHBV‐ALF. Sera were available on 47 and 23 patients, respectively. A quantitative immunoassay was used to determine IgM anti‐HBc levels, and real‐time polymerase chain reaction (rtPCR) was used to determine HBV VLs. AHBV‐ALFs had much higher IgM anti‐HBc titers than CHBV‐ALFs (signal‐to‐noise [S/N] ratio median: 88.5; range, 0‐1,120 versus 1.3, 0‐750; P < 0.001); a cut point for a S/N ratio of 5.0 correctly identified 44 of 46 (96%) AHBV‐ALFs and 16 of 23 (70%) CHBV‐ALFs; the area under the receiver operator characteristic curve was 0.86 (P < 0.001). AHBV‐ALF median admission VL was 3.9 (0‐8.1) log10 IU/mL versus 5.2 (2.0‐8.7) log10 IU/mL for CHBV‐ALF (P < 0.025). Twenty percent (12 of 60) of the AHBV‐ALF group had no hepatitis B surface antigen (HBsAg) detectable on admission to study, wheras no CHBV‐ALF patients experienced HBsAg clearance. Rates of transplant‐free survival were 33% (20 of 60) for AHBV‐ALF versus 11% (3 of 27) for CHBV‐ALF (P = 0.030). Conclusions: AHBV‐ALF and CHBV‐ALF differ markedly in IgM anti‐HBc titers, in HBV VLs, and in prognosis, suggesting that the two forms are, indeed, different entities that might each have a unique pathogenesis. (HEPATOLOGY 2011) |
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| AbstractList | UNLABELLEDHepatitis B virus (HBV)-related acute liver failure (HBV-ALF) may occur after acute HBV infection (AHBV-ALF) or during an exacerbation of chronic HBV infection (CHBV-ALF). Clinical differentiation of the two is often difficult if a previous history of HBV is not available. Quantitative measurements of immunoglobulin M (IgM) anti-hepatitis B core antibody (anti-HBc) titers and of HBV viral loads (VLs) might allow the separation of AHBV-ALF from CHBV-ALF. Of 1,602 patients with ALF, 60 met clinical criteria for AHBV-ALF and 27 for CHBV-ALF. Sera were available on 47 and 23 patients, respectively. A quantitative immunoassay was used to determine IgM anti-HBc levels, and real-time polymerase chain reaction (rtPCR) was used to determine HBV VLs. AHBV-ALFs had much higher IgM anti-HBc titers than CHBV-ALFs (signal-to-noise [S/N] ratio median: 88.5; range, 0-1,120 versus 1.3, 0-750; P < 0.001); a cut point for a S/N ratio of 5.0 correctly identified 44 of 46 (96%) AHBV-ALFs and 16 of 23 (70%) CHBV-ALFs; the area under the receiver operator characteristic curve was 0.86 (P < 0.001). AHBV-ALF median admission VL was 3.9 (0-8.1) log10 IU/mL versus 5.2 (2.0-8.7) log10 IU/mL for CHBV-ALF (P < 0.025). Twenty percent (12 of 60) of the AHBV-ALF group had no hepatitis B surface antigen (HBsAg) detectable on admission to study, wheras no CHBV-ALF patients experienced HBsAg clearance. Rates of transplant-free survival were 33% (20 of 60) for AHBV-ALF versus 11% (3 of 27) for CHBV-ALF (P = 0.030). CONCLUSIONSAHBV-ALF and CHBV-ALF differ markedly in IgM anti-HBc titers, in HBV VLs, and in prognosis, suggesting that the two forms are, indeed, different entities that might each have a unique pathogenesis. Hepatitis B virus (HBV)-related acute liver failure (HBV-ALF) may occur after acute HBV infection (AHBV-ALF) or during an exacerbation of chronic HBV infection (CHBV-ALF). Clinical differentiation of the two is often difficult if a previous history of HBV is not available. Quantitative measurements of immunoglobulin M (IgM) anti–hepatitis B core antibody (anti-HBc) titers and of HBV viral loads (VLs) might allow the separation of AHBV-ALF from CHBV-ALF. Of 1,602 patients with ALF, 60 met clinical criteria for AHBV-ALF and 27 for CHBV-ALF. Sera were available on 47 and 23 patients, respectively. A quantitative immunoassay was used to determine IgM anti-HBc levels, and real-time polymerase chain reaction (rtPCR) was used to determine HBV VLs. AHBV-ALFs had much higher IgM anti-HBc titers than CHBV-ALFs (signal-to-noise [S/N] ratio median: 88.5; range, 0-1,120 versus 1.3, 0-750; P < 0.001); a cut point for a S/N ratio of 5.0 correctly identified 44 of 46 (96%) AHBV-ALFs and 16 of 23 (70%) CHBV-ALFs; the area under the receiver operator characteristic curve was 0.86 ( P < 0.001). AHBV-ALF median admission VL was 3.9 (0-8.1) log10 IU/mL versus 5.2 (2.0-8.7) log10 IU/mL for CHBV-ALF ( P < 0.025). Twenty percent (12 of 60) of the AHBV-ALF group had no hepatitis B surface antigen (HBsAg) detectable on admission to study, wheras no CHBV-ALF patients experienced HBsAg clearance. Rates of transplant-free survival were 33% (20 of 60) for AHBV-ALF versus 11% (3 of 27) for CHBV-ALF ( P = 0.030). Conclusions: AHBV-ALF and CHBV-ALF differ markedly in IgM anti-HBc titers, in HBV VLs, and in prognosis, suggesting that the two forms are, indeed, different entities that might each have a unique pathogenesis. Hepatitis B virus (HBV)‐related acute liver failure (HBV‐ALF) may occur after acute HBV infection (AHBV‐ALF) or during an exacerbation of chronic HBV infection (CHBV‐ALF). Clinical differentiation of the two is often difficult if a previous history of HBV is not available. Quantitative measurements of immunoglobulin M (IgM) anti–hepatitis B core antibody (anti‐HBc) titers and of HBV viral loads (VLs) might allow the separation of AHBV‐ALF from CHBV‐ALF. Of 1,602 patients with ALF, 60 met clinical criteria for AHBV‐ALF and 27 for CHBV‐ALF. Sera were available on 47 and 23 patients, respectively. A quantitative immunoassay was used to determine IgM anti‐HBc levels, and real‐time polymerase chain reaction (rtPCR) was used to determine HBV VLs. AHBV‐ALFs had much higher IgM anti‐HBc titers than CHBV‐ALFs (signal‐to‐noise [S/N] ratio median: 88.5; range, 0‐1,120 versus 1.3, 0‐750; P < 0.001); a cut point for a S/N ratio of 5.0 correctly identified 44 of 46 (96%) AHBV‐ALFs and 16 of 23 (70%) CHBV‐ALFs; the area under the receiver operator characteristic curve was 0.86 (P < 0.001). AHBV‐ALF median admission VL was 3.9 (0‐8.1) log10 IU/mL versus 5.2 (2.0‐8.7) log10 IU/mL for CHBV‐ALF (P < 0.025). Twenty percent (12 of 60) of the AHBV‐ALF group had no hepatitis B surface antigen (HBsAg) detectable on admission to study, wheras no CHBV‐ALF patients experienced HBsAg clearance. Rates of transplant‐free survival were 33% (20 of 60) for AHBV‐ALF versus 11% (3 of 27) for CHBV‐ALF (P = 0.030). Conclusions: AHBV‐ALF and CHBV‐ALF differ markedly in IgM anti‐HBc titers, in HBV VLs, and in prognosis, suggesting that the two forms are, indeed, different entities that might each have a unique pathogenesis. (HEPATOLOGY 2011) Hepatitis B virus (HBV)-related acute liver failure (HBV-ALF) may occur after acute HBV infection (AHBV-ALF) or during an exacerbation of chronic HBV infection (CHBV-ALF). Clinical differentiation of the two is often difficult if a previous history of HBV is not available. Quantitative measurements of immunoglobulin M (IgM) anti-hepatitis B core antibody (anti-HBc) titers and of HBV viral loads (VLs) might allow the separation of AHBV-ALF from CHBV-ALF. Of 1,602 patients with ALF, 60 met clinical criteria for AHBV-ALF and 27 for CHBV-ALF. Sera were available on 47 and 23 patients, respectively. A quantitative immunoassay was used to determine IgM anti-HBc levels, and real-time polymerase chain reaction (rtPCR) was used to determine HBV VLs. AHBV-ALFs had much higher IgM anti-HBc titers than CHBV-ALFs (signal-to-noise [S/N] ratio median: 88.5; range, 0-1,120 versus 1.3, 0-750; P < 0.001); a cut point for a S/N ratio of 5.0 correctly identified 44 of 46 (96%) AHBV-ALFs and 16 of 23 (70%) CHBV-ALFs; the area under the receiver operator characteristic curve was 0.86 (P < 0.001). AHBV-ALF median admission VL was 3.9 (0-8.1) log10 IU/mL versus 5.2 (2.0-8.7) log10 IU/mL for CHBV-ALF (P < 0.025). Twenty percent (12 of 60) of the AHBV-ALF group had no hepatitis B surface antigen (HBsAg) detectable on admission to study, wheras no CHBV-ALF patients experienced HBsAg clearance. Rates of transplant-free survival were 33% (20 of 60) for AHBV-ALF versus 11% (3 of 27) for CHBV-ALF (P = 0.030). AHBV-ALF and CHBV-ALF differ markedly in IgM anti-HBc titers, in HBV VLs, and in prognosis, suggesting that the two forms are, indeed, different entities that might each have a unique pathogenesis. |
| Author | Yuan, He-Jun Word, R. Ann Dao, Doan Y. Lok, Anna S.F. Attar, Nahid Hynan, Linda S. Balko, Jody Sanders, Corron Lee, William M. |
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| Copyright | Copyright © 2011 American Association for the Study of Liver Diseases 2015 INIST-CNRS Copyright © 2011 American Association for the Study of Liver Diseases. |
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| DOI | 10.1002/hep.24732 |
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| Keywords | Immunoglobulins Antibody Acute Orthohepadnavirus Hepatic disease Infection Virus Viral hepatitis B Liver failure Hepadnaviridae Viral disease DNA Gastroenterology Digestive diseases Serum Hepatitis B virus Subtype Quantitative analysis |
| Language | English |
| License | CC BY 4.0 Copyright © 2011 American Association for the Study of Liver Diseases. |
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| Notes | Potential conflict of interest: Dr. Lee consults for and received grants from Novartis. He consults for Eli Lilly. He also received grants from Bristol-Myers Squibb, Siemens, Merck, Gilead, and Boehringer-Ingelheim. ark:/67375/WNG-PMPQ756L-M ArticleID:HEP24732 Members of the Acute Liver Failure Study Group are listed in the Appendix. istex:2A5A9E077FA6C7F35491498BA826192EA8E28946 This study was funded by a National Institutes of Health grant (DK U-01 58369) for the Acute Liver Failure Study Group provided by the National Institute of Diabetes and Digestive and Kidney Diseases. Additional funding was provided by the Tips Fund of the Northwestern Medical Foundation, the Jeanne Roberts and Rollin and Mary Ella King Funds of the Southwestern Medical Foundation, and T-32 DK007745-12 (to D.D.). Potential conflict of interest: Dr. Lee consults for and received grants from Novartis. He consults for Eli Lilly. He also received grants from Bristol‐Myers Squibb, Siemens, Merck, Gilead, and Boehringer‐Ingelheim. fax: 214‐645‐6114 This study was funded by a National Institutes of Health grant (DK U‐01 58369) for the Acute Liver Failure Study Group provided by the National Institute of Diabetes and Digestive and Kidney Diseases. Additional funding was provided by the Tips Fund of the Northwestern Medical Foundation, the Jeanne Roberts and Rollin and Mary Ella King Funds of the Southwestern Medical Foundation, and T‐32 DK007745‐12 (to D.D.). ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
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| References_xml | – volume: 5 start-page: 10 year: 1985 end-page: 13 article-title: Hepatitis B virus DNA in serum from patients with acute hepatitis B publication-title: Hepatology – volume: 84 start-page: 604 year: 1983 end-page: 610 article-title: Immunoglobulin M antibody against hepatitis B core antigen for the diagnosis of fulminant type B hepatitis publication-title: Gastroenterology – volume: 25 start-page: 644 year: 1996 end-page: 648 article-title: Quantitative analysis of IgM anti‐HBc in chronic hepatitis B patients using a new “gray‐zone” for the evaluation of borderline” values publication-title: J Hepatol – volume: 44 start-page: 326 year: 2006 end-page: 334 article-title: Influence of genotypes and precore mutations on fulminant or chronic outcome of acute hepatitis B virus infection publication-title: Hepatology – volume: 93 start-page: 550 year: 1994 end-page: 555 article-title: Hepatitis B virus precore mutation and fulminant hepatitis in the United States. A polymerase chain reaction‐based assay for the detection of specific mutation publication-title: J Clin Invest – volume: 17 start-page: 10 year: 1976 end-page: 13 article-title: Hepatitis B antigen (HBsAg) and/or antibodies (anti‐HBs and anti‐HBc) in fulminant hepatitis: pathogenic and prognostic significance publication-title: Gut – volume: 329 start-page: 1862 year: 1993 end-page: 1872 article-title: Acute liver failure publication-title: N Engl J Med – volume: 89 start-page: 252 year: 1985 end-page: 258 article-title: Immunoglobulin M antibody to hepatitis B core antigen in patients with chronic type B hepatitis publication-title: Gastroenterology – volume: 47 start-page: e52 year: 2008 end-page: e56 article-title: Mortality secondary to fulminant hepatic failure in patients with prior resolution of hepatitis B virus infection in Japan publication-title: Clin Infect Dis – volume: 337 start-page: 1733 year: 1997 end-page: 1745 article-title: Hepatitis B virus infection publication-title: N Engl J Med – volume: 126 start-page: 207 year: 2005 end-page: 213 article-title: Real‐time PCR quantitation of hepatitis B virus DNA using automated sample preparation and murine cytomegalovirus internal control publication-title: J Virol Methods – volume: 64 start-page: 1298 year: 1990 end-page: 1303 article-title: Hepatitis B viruses with precore region defects prevail in persistently infected hosts along with seroconversion to the antibody against e antigen publication-title: J Virol – volume: 49 start-page: S156 year: 2009 end-page: S165 article-title: Reactivation of hepatitis B publication-title: Hepatology – volume: 179 start-page: 5877 year: 2007 end-page: 5885 article-title: B cell activation state‐governed formation of germinal centers following viral infection publication-title: J Immunol – volume: 2 start-page: 669 year: 1976 end-page: 671 article-title: Enhanced HBsAb production in pathogenesis of fulminant viral hepatitis type B publication-title: Br Med J – volume: 37 start-page: 593 year: 2003 end-page: 597 article-title: Role of hepatitis B virus genotypes in chronic hepatitis B exacerbation publication-title: Clin Infect Dis – volume: 55 start-page: 35 year: 1998 end-page: 41 article-title: Clinical and molecular virological differences between fulminant hepatic failures following acute and chronic infection with hepatitis B virus publication-title: J Med Virol – volume: 118 start-page: 554 year: 2000 end-page: 559 article-title: Hepatitis B genotypes correlate with clinical outcomes in patients with chronic hepatitis B publication-title: Gastroenterology – volume: 45 start-page: 1056 year: 2007 end-page: 1075 article-title: Management of hepatitis B: summary of a clinical research workshop publication-title: Hepatology – volume: 120 start-page: 1009 year: 2001 end-page: 1022 article-title: Acute flares in chronic hepatitis B: the natural and unnatural history of an immunologically mediated liver disease publication-title: Gastroenterology – volume: 21 start-page: 859 year: 2006 end-page: 862 article-title: Higher cut‐off index value of immunoglobulin M antibody to hepatitis B core antigen in Taiwanese patients with hepatitis B publication-title: J Gastroenterol Hepatol |
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| Snippet | Hepatitis B virus (HBV)‐related acute liver failure (HBV‐ALF) may occur after acute HBV infection (AHBV‐ALF) or during an exacerbation of chronic HBV infection... Hepatitis B virus (HBV)-related acute liver failure (HBV-ALF) may occur after acute HBV infection (AHBV-ALF) or during an exacerbation of chronic HBV infection... UNLABELLEDHepatitis B virus (HBV)-related acute liver failure (HBV-ALF) may occur after acute HBV infection (AHBV-ALF) or during an exacerbation of chronic HBV... |
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| SubjectTerms | Adolescent Adult Aged Antibodies, Anti-Idiotypic - blood Biological and medical sciences Deoxyribonucleic acid Diagnosis, Differential DNA DNA, Viral - blood Female Gastroenterology. Liver. Pancreas. Abdomen Genotype Hepatitis Hepatitis B Hepatitis B Antibodies - blood Hepatitis B Core Antigens - blood Hepatitis B Core Antigens - immunology Hepatitis B virus Hepatitis B virus - genetics Hepatitis B virus - immunology Hepatitis B virus - isolation & purification Hepatitis B, Chronic - blood Hepatitis B, Chronic - complications Hepatology Human viral diseases Humans Immunoglobulin M - blood Immunoglobulins Infectious diseases Liver - pathology Liver - virology Liver Failure, Acute - classification Liver Failure, Acute - diagnosis Liver Failure, Acute - virology Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical prognosis Medical sciences Middle Aged Other diseases. Semiology Prognosis Prospective Studies Retrospective Studies Viral diseases Viral hepatitis Young Adult |
| Title | Two distinct subtypes of hepatitis B virus-related acute liver failure are separable by quantitative serum immunoglobulin M anti-hepatitis B core antibody and hepatitis B virus DNA levels |
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