Archives

  • 2018-07
  • 2019-04
  • 2019-05
  • 2019-06
  • 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2019-12
  • 2020-01
  • 2020-02
  • 2020-03
  • 2020-04
  • 2020-05
  • 2020-06
  • 2020-07
  • 2020-08
  • 2020-09
  • 2020-10
  • 2020-11
  • 2020-12
  • 2021-01
  • 2021-02
  • 2021-03
  • 2021-04
  • 2021-05
  • 2021-06
  • 2021-07
  • 2021-08
  • 2021-09
  • 2021-10
  • 2021-11
  • 2021-12
  • 2022-01
  • 2022-02
  • 2022-03
  • 2022-04
  • 2022-05
  • 2022-06
  • 2022-07
  • 2022-08
  • 2022-09
  • 2022-10
  • 2022-11
  • 2022-12
  • 2023-01
  • 2023-02
  • 2023-03
  • 2023-04
  • 2023-05
  • 2023-06
  • 2023-07
  • 2023-08
  • 2023-09
  • 2023-10
  • 2023-11
  • 2023-12
  • 2024-01
  • 2024-02
  • 2024-03
  • 2024-04

    • br Ethical approve and consent to

    2021-10-21


    Ethical approve and consent to participate
    Consent for publication
    Availability of supporting data
    Competing interests
    Funding This work was supported by a grant from Key Program of National Natural Science Foundation of China (No. 81330089) and the Shanghai Science and Technology Funds (Nos. 17ZR1401700).
    Authors' contributions The following are the supplementary data related to this article.
    Transparency document
    Acknowledgements
    Introduction HBV reactivation is a common complication that may lead to a life-threatening liver decompensation in patients with chronic HBV infection (HBsAg positive) who receive cytotoxic or immunosuppressive therapy. Prophylactic antiviral therapy is recommended for this patient ZSTK474 by guidelines of HBV management.[1], [2], [3], [4] For patients with resolved HBV infection (HBsAg negative and anti-HBV core antibody [anti-HBc] positive), HBV reactivation is best characterized in patients with lymphoma who are treated with B cell-depleting agents, such as rituximab, and the incidence of HBV reactivation ranged from about 10% to 30%.[5], [6], [7], [8], [9] Prophylactic antiviral therapy has been demonstrated to reduce the incidence of HBV reactivation in patients with lymphoma and resolved HBV infection who received rituximab-containing chemotherapy, and is recommended by most clinical practice guidelines.[1], [2], [3], [4] Alternatively, the patients can be followed up regularly by monitoring HBV DNA and alanine aminotransferase (ALT) levels every 1–3 months, and start antiviral therapy upon HBV reactivation.[7], [8] In HBV endemic area, either prophylactic antiviral therapy or regular HBV DNA monitoring may cause significant burden on health resource allocation because approximately 60% of the adult population has resolved HBV infections. Therefore, the identification of high-risk patients for HBV reactivation will help in the optimization of a preventive strategy and resource allocation. Low or absent anti-HBV surface antibody (anti-HBs) at baseline was the best characterized risk factor of HBV reactivation in a previous series of patients with lymphoma and resolved HBV infection.[6], [7], [8], [9] However, the diagnosis criteria of HBV reactivation varied in previous studies, and some reported HBV reactivations may represent a transient HBV DNA increase that is not clinically significant. Exploration of markers that may help predict the clinical outcome of HBV reactivation will further focus the limited health-care resources to the most vulnerable patient groups. The positivity of anti-HBc antibodies was used to be a marker of past HBV infections. Recently, the quantification of anti-HBc levels by using a newly developed double-sandwich immunoassay has emerged as a new marker of chronic HBV infection.[11], [12] In the natural history of HBV infection, patients in the phases with hepatitis activity (the immune clearance and HBeAg-negative hepatitis phases) have higher anti-HBc levels than those in the immune tolerant or the inactive carrier phases.[13], [14] Anti-HBc levels were well correlated with ALT levels, an indicator of liver injury, and associated with the natural history and treatment response of HBV infection.[13], [14], [15], [16] In patients who received interferon or nucleos(t)ide analogue treatment, those with higher anti-HBc levels had a higher chance of HBeAg seroconversion than those with lower anti-HBc. In patients with resolved HBV infection, the anti-HBc levels were higher in those with detectable serum HBV DNA (occult HBV infection) than those without detectable HBV DNA (past HBV infection only). This suggests that anti-HBc levels may reflect the residual HBV replication in patients with resolved HBV infection. Therefore, we hypothesized that the quantitation of anti-HBc levels may be a marker indicating residual HBV load and may help predict the risk of HBV reactivation in patients with lymphoma and resolved HBV infection who received rituximab-containing chemotherapy. In this study, we tested this hypothesis by analyzing the serum samples obtained from a prospective cohort study, and explored the value of baseline anti-HBc and anti-HBs levels for the prediction of HBV reactivation and clinical outcome.