Early serum HBsAg drop: A strong predictor of sustained virological response to pegylated interferon alfa‐2a in HBeAg‐negative patients

Pegylated interferon alfa‐2a (PEG‐IFN) may induce sustained virological response (SVR) in 20% of hepatitis B e antigen (HBeAg)‐negative chronic hepatitis B (CHB) patients. In addition, loss of hepatitis B surface antigen (HBsAg) is achieved with a 10% yearly rate after treatment cessation in sustain...

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Veröffentlicht in:Hepatology (Baltimore, Md.) Md.), 2009-04, Vol.49 (4), p.1151-1157
Hauptverfasser: Moucari, Rami, Mackiewicz, Vincent, Lada, Olivier, Ripault, Marie‐Pierre, Castelnau, Corinne, Martinot‐Peignoux, Michelle, Dauvergne, Agnes, Asselah, Tarik, Boyer, Nathalie, Bedossa, Pierre, Valla, Dominique, Vidaud, Michel, Nicolas‐Chanoine, Marie‐Hélène, Marcellin, Patrick
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container_issue 4
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container_title Hepatology (Baltimore, Md.)
container_volume 49
creator Moucari, Rami
Mackiewicz, Vincent
Lada, Olivier
Ripault, Marie‐Pierre
Castelnau, Corinne
Martinot‐Peignoux, Michelle
Dauvergne, Agnes
Asselah, Tarik
Boyer, Nathalie
Bedossa, Pierre
Valla, Dominique
Vidaud, Michel
Nicolas‐Chanoine, Marie‐Hélène
Marcellin, Patrick
description Pegylated interferon alfa‐2a (PEG‐IFN) may induce sustained virological response (SVR) in 20% of hepatitis B e antigen (HBeAg)‐negative chronic hepatitis B (CHB) patients. In addition, loss of hepatitis B surface antigen (HBsAg) is achieved with a 10% yearly rate after treatment cessation in sustained responders. The aim of this study was to assess on‐treatment serum HBsAg kinetics to predict SVR in HBeAg‐negative patients treated with PEG‐IFN. Forty‐eight consecutive patients were treated with PEG‐IFN (180 μg/week) for 48 weeks. Serum hepatitis B virus (HBV) DNA (COBAS TaqMan) and HBsAg (Abbott Architect HBsAg QT assay) were assessed at baseline, during treatment (weeks 12, 24, and 48), and during follow‐up (weeks 72 and 96). SVR was defined as undetectable serum HBV DNA (
doi_str_mv 10.1002/hep.22744
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In addition, loss of hepatitis B surface antigen (HBsAg) is achieved with a 10% yearly rate after treatment cessation in sustained responders. The aim of this study was to assess on‐treatment serum HBsAg kinetics to predict SVR in HBeAg‐negative patients treated with PEG‐IFN. Forty‐eight consecutive patients were treated with PEG‐IFN (180 μg/week) for 48 weeks. Serum hepatitis B virus (HBV) DNA (COBAS TaqMan) and HBsAg (Abbott Architect HBsAg QT assay) were assessed at baseline, during treatment (weeks 12, 24, and 48), and during follow‐up (weeks 72 and 96). SVR was defined as undetectable serum HBV DNA (&lt;70 copies/mL) 24 weeks after treatment cessation. Twenty‐five percent of patients achieved SVR. They were not different from those who failed treatment regarding age, sex, ethnicity, HBV genotype, baseline serum HBV DNA and HBsAg levels, or liver histology. During treatment, serum HBsAg levels decreased only in patients who developed SVR, with mean decreases of 0.8 ± 0.5, 1.5 ± 0.6, and 2.1 ± 1.2 log10 IU/mL at weeks 12, 24, and 48, respectively. A decrease of 0.5 and 1 log10 IU/mL in serum HBsAg levels at weeks 12 and 24 of therapy, respectively, had high predictive values of SVR (negative predictive value [NPV] 90%, positive predictive value [PPV] 89% for week 12; NPV 97%, PPV 92% for week 24). HBsAg loss was observed in three patients, all with SVR. Conclusion: Early serum HBsAg drop has high predictive values of SVR to PEG‐IFN in HBeAg‐negative CHB patients. Serum quantitative HBsAg may be a useful tool to optimize the management of PEG‐IFN therapy in these patients. 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In addition, loss of hepatitis B surface antigen (HBsAg) is achieved with a 10% yearly rate after treatment cessation in sustained responders. The aim of this study was to assess on‐treatment serum HBsAg kinetics to predict SVR in HBeAg‐negative patients treated with PEG‐IFN. Forty‐eight consecutive patients were treated with PEG‐IFN (180 μg/week) for 48 weeks. Serum hepatitis B virus (HBV) DNA (COBAS TaqMan) and HBsAg (Abbott Architect HBsAg QT assay) were assessed at baseline, during treatment (weeks 12, 24, and 48), and during follow‐up (weeks 72 and 96). SVR was defined as undetectable serum HBV DNA (&lt;70 copies/mL) 24 weeks after treatment cessation. Twenty‐five percent of patients achieved SVR. They were not different from those who failed treatment regarding age, sex, ethnicity, HBV genotype, baseline serum HBV DNA and HBsAg levels, or liver histology. During treatment, serum HBsAg levels decreased only in patients who developed SVR, with mean decreases of 0.8 ± 0.5, 1.5 ± 0.6, and 2.1 ± 1.2 log10 IU/mL at weeks 12, 24, and 48, respectively. A decrease of 0.5 and 1 log10 IU/mL in serum HBsAg levels at weeks 12 and 24 of therapy, respectively, had high predictive values of SVR (negative predictive value [NPV] 90%, positive predictive value [PPV] 89% for week 12; NPV 97%, PPV 92% for week 24). HBsAg loss was observed in three patients, all with SVR. Conclusion: Early serum HBsAg drop has high predictive values of SVR to PEG‐IFN in HBeAg‐negative CHB patients. Serum quantitative HBsAg may be a useful tool to optimize the management of PEG‐IFN therapy in these patients. (HEPATOLOGY 2009.)</description><subject>Adult</subject><subject>Antiviral Agents - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>DNA, Viral - blood</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. 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In addition, loss of hepatitis B surface antigen (HBsAg) is achieved with a 10% yearly rate after treatment cessation in sustained responders. The aim of this study was to assess on‐treatment serum HBsAg kinetics to predict SVR in HBeAg‐negative patients treated with PEG‐IFN. Forty‐eight consecutive patients were treated with PEG‐IFN (180 μg/week) for 48 weeks. Serum hepatitis B virus (HBV) DNA (COBAS TaqMan) and HBsAg (Abbott Architect HBsAg QT assay) were assessed at baseline, during treatment (weeks 12, 24, and 48), and during follow‐up (weeks 72 and 96). SVR was defined as undetectable serum HBV DNA (&lt;70 copies/mL) 24 weeks after treatment cessation. Twenty‐five percent of patients achieved SVR. They were not different from those who failed treatment regarding age, sex, ethnicity, HBV genotype, baseline serum HBV DNA and HBsAg levels, or liver histology. During treatment, serum HBsAg levels decreased only in patients who developed SVR, with mean decreases of 0.8 ± 0.5, 1.5 ± 0.6, and 2.1 ± 1.2 log10 IU/mL at weeks 12, 24, and 48, respectively. A decrease of 0.5 and 1 log10 IU/mL in serum HBsAg levels at weeks 12 and 24 of therapy, respectively, had high predictive values of SVR (negative predictive value [NPV] 90%, positive predictive value [PPV] 89% for week 12; NPV 97%, PPV 92% for week 24). HBsAg loss was observed in three patients, all with SVR. Conclusion: Early serum HBsAg drop has high predictive values of SVR to PEG‐IFN in HBeAg‐negative CHB patients. Serum quantitative HBsAg may be a useful tool to optimize the management of PEG‐IFN therapy in these patients. (HEPATOLOGY 2009.)</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>19115222</pmid><doi>10.1002/hep.22744</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
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subjects Adult
Antiviral Agents - therapeutic use
Biological and medical sciences
DNA, Viral - blood
Female
Gastroenterology. Liver. Pancreas. Abdomen
Hepatitis B e Antigens - blood
Hepatitis B Surface Antigens - blood
Hepatitis B, Chronic - drug therapy
Hepatitis B, Chronic - immunology
Humans
Interferon-alpha - therapeutic use
Liver. Biliary tract. Portal circulation. Exocrine pancreas
Male
Medical sciences
Middle Aged
Polyethylene Glycols - therapeutic use
Predictive Value of Tests
Recombinant Proteins
title Early serum HBsAg drop: A strong predictor of sustained virological response to pegylated interferon alfa‐2a in HBeAg‐negative patients
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