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Review
. 2015 Jul;22(3):360-5.
doi: 10.1177/107327481502200315.

Association of Lymphomagenesis and the Reactivation of Hepatitis B Virus in Non-Hodgkin Lymphoma

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Free article
Review

Association of Lymphomagenesis and the Reactivation of Hepatitis B Virus in Non-Hodgkin Lymphoma

Samir Dalia et al. Cancer Control. 2015 Jul.
Free article

Abstract

Background: Hepatitis B virus (HBV) has been associated with the development of non-Hodgkin lymphoma (NHL) and can be reactivated in patients being treated for NHL.

Methods: Articles published between 2000 and 2015 that discussed an association between NHL and HBV, mechanisms of HBV induction of NHL, and HBV reactivation in patients with NHL were reviewed and the results compiled to help health care professionals better understand the risk of developing NHL in HBV-seropositive individuals, describe potential etiologies by which HBV infection may lead to lymphomagenesis, and highlight the recent medical literature with respect to the reactivation of HBV in the setting of NHL.

Results: An association exists between HBV infection and NHL development. Immunosuppression due to HBV, chronic viral stimulation, and dysregulation of the immune system are possible ways in which lymphoma can develop in patients with HBV infection. All patients being treated with anti-CD20 antibodies or those from or living in HBV-endemic regions should be tested for hepatitis B surface antigen, core antibody, and surface antibody prior to initiating therapy. HBV DNA polymerase chain reaction (PCR) may also be useful in certain cases. Among HBV-seropositive patients or those with detectable HBV DNA, prophylaxis with an antiviral agent should be initiated for 1 year after NHL therapy. HBV DNA PCR monitoring should be undertaken each month during the course of treatment and every 3 months after treatment for a 1-year duration.

Conclusions: Health care professionals should become more comfortable treating these high-risk patients with NHL as they become more informed about potential lymphomagenesis and the reactivation of HBV.

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