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Editorials |5 January 2016

Evaluating Hepatitis B Virus Reactivation During Solid Tumor Chemotherapy: Evidence to Guide Pretreatment Hepatitis B Screening and Prophylaxis

Vincent Lo Re III, MD, MSCE; Mindy Schuster, MD, MSCE

Article, Author, and Disclosure Information
Author, Article, and Disclosure Information
This article was published online first at www.annals.org on 24 November 2015.
  • From University of Pennsylvania, Philadelphia, Pennsylvania.

    Disclosures: Disclosures can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M15-2722.

    Requests for Single Reprints: Vincent Lo Re III, MD, MSCE, Center for Clinical Epidemiology and Biostatistics, Perelman School of Medicine, University of Pennsylvania, 836 Blockley Hall, 423 Guardian Drive, Philadelphia, PA 19104; e-mail, vincentl@mail.med.upenn.edu.

    Current Author Addresses: Dr. Lo Re: Center for Clinical Epidemiology and Biostatistics, Perelman School of Medicine, University of Pennsylvania, 836 Blockley Hall, 423 Guardian Drive, Philadelphia, PA 19104.

    Dr. Schuster: Division of Infectious Diseases, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, 3 Silverstein, Suite E, 3400 Spruce Street, Philadelphia, PA 19104.

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Reactivation of hepatitis B virus (HBV) infection is increasingly recognized as a complication of immunosuppressive therapy, particularly chemotherapy. It is characterized by an abrupt increase in HBV DNA level among patients with positive hepatitis B surface antigen (HBsAg) or the reappearance of serum HBV DNA in those with serologic evidence of resolved infection (negative HBsAg and positive core antibody [HBcAb] with or without HBV surface antibody). It is usually accompanied by elevations in liver aminotransferase levels. Reactivation can lead to serious hepatic injury, chemotherapy interruption, liver failure, and death (1).
Reactivation of HBV occurs because after infection, the virus establishes covalently closed circular DNA as a durable miniature chromosome within the nuclei of infected hepatocytes during replication. Because HBV closed circular DNA persists, even after serologic resolution of infection, acquired immunosuppression can disrupt the ability of the host immune system to control HBV replication and result in reactivation.
More than 248 million persons worldwide have chronic HBV infection and may receive immunosuppressive therapy for cancer, autoimmune disease, or organ transplantation, which puts them at risk for HBV reactivation. Prophylactic treatment can substantially reduce this risk in at-risk patients receiving chemotherapy (2).
Recent meta-analyses (3) show that use of B-cell–depleting agents (rituximab or ofatumumab) in hematologic tumors is associated with a particularly high risk for HBV reactivation. Therefore, the U.S. Food and Drug Administration issued a drug safety communication (4) urging health care providers to screen all patients for HBV infection before starting...
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Lo Re V, Schuster M. Evaluating Hepatitis B Virus Reactivation During Solid Tumor Chemotherapy: Evidence to Guide Pretreatment Hepatitis B Screening and Prophylaxis. Ann Intern Med. 2016;164:64–65. [Epub ahead of print 24 November 2015]. doi: https://doi.org/10.7326/M15-2722

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Published: Ann Intern Med. 2016;164(1):64-65.

DOI: 10.7326/M15-2722

Published at www.annals.org on 24 November 2015

6 Citations

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