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. 2008 Jun;2(2):152-62.
doi: 10.1007/s12072-008-9056-3. Epub 2008 Mar 5.

Hepatitis B reactivation after chemotherapy: two decades of clinical research

George K K Lau  1
Affiliations

Hepatitis B reactivation after chemotherapy: two decades of clinical research

George K K Lau. Hepatol Int. 2008 Jun.

Abstract

Hepatitis due to hepatitis B virus reactivation after cytotoxic or immunosuppressive therapy is a serious cause of liver-related morbidity and mortality. With the characterization of the underlying pathogenesis, much progress in the management of this important clinical problem has been made in the past 2 decades. By year 2008, it is mandatory to screen for hepatitis B surface antigen status before initiating intensive chemotherapy or immunosuppressive therapy. All those who are hepatitis B surface antigen positive should be started on preemptive nucleos(t)ide analogues. However, there remains important issues, such as the type and duration of nucleos(t)ide analogue therapy, which need to be understood. As not all hepatitis B surface antigen-positive patients will suffer from HBV reactivation, it is therefore useful to identify risk factors related to HBV reactivation so that patients will not be treated unnecessarily with nucleos(t)ide analogues. To date, a high baseline level of viral replication, as reflected by high serum HBV DNA level, positive serum hepatitis B e antigen, and a high intrahepatic covalently closed circular DNA level, is the most important predictor for HBV reactivation. Recently, there has been an increased awareness of reactivation of occult hepatitis B virus, especially in hepatitis B virus endemic area, such as the Asia-Pacific region. Careful epidemiological study will be needed to clarify the impact of occult hepatitis B infection in patients treated with cytotoxic or immunosuppressive therapy.

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Figures

Fig. 1
Fig. 1
Hepatitis due to HBV reactivation is a 2-phase process. The initial phase is related to intense immunosuppression caused by the cytotoxic therapy and is characterized by an enhanced HBV viral replication. There is a marked increase in serum HBV DNA level and viral protein expression in the hepatocytes. The second phase occurs during immune restoration on withdrawal of the chemotherapy and is marked by a much enhanced host immune response against HBV-laden hepatocytes, resulting in liver damages of varying severity, from hepatitis to hepatic failure and even death (solid line). The use of nucleoside analogues with anti-HBV activity in the initial phase could effectively prevent viral replication enhancement and therefore reduce the incidence of HBV-related hepatitis (dotted line)
Fig. 2
Fig. 2
A meta-analysis of 13 studies reported during 2002–2006 that compare preemptive use of lamivudine versus historical controls in hepatitis B surface antigen-positive patients treated with systemic chemotherapy or transhepatic intraarterial chemotherapy. Altogether, 702 hepatitis B surface antigen-positive patients (237 treated with preemptive lamivudine and 465 untreated controls) were recruited. Those patients treated with preemptive lamivudine had a significantly lower incidence of hepatitis due to HBV reactivation (3.3%) than the untreated controls (35.0%; OR 0.083; 95% CI: 0.045–0.155; p < 0.0001). Hence, there is a strong suggestion of a beneficial effect on the administration of preemptive lamivudine in reducing the hepatitis due to HBV reactivation in HBsAg-positive patients treated with cytotoxic or immunosuppressive therapy
Fig. 3
Fig. 3
Algorithm for management of hepatitis B surface antigen-positive patients treated with a cytotoxic or immunosuppressive agent. HBsAg, hepatitis B surface antigen; HBeAg, hepatitis B e antigen
See this image and copyright information in PMC

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