Lamivudine therapy for prevention of immunosuppressive-induced hepatitis B virus reactivation in hepatitis B surface antigen carriers

Shibolet, Oren; Ilan, Yaron; Gillis, Shmuel; Hubert, Ayala; Shouval, Daniel; Safadi, Rifaat

doi:10.1182/blood.v100.2.391

Cited by 143 publications

(106 citation statements)

References 39 publications

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“…Prophylactic treatment with antiviral nucleotide analogue lamivudine prior to the start of chemotherapy has been suggested to be effective in reducing the incidence of HBV reactivation (Rossi et al, 2001;Liao et al, 2002;Lim et al, 2002;Persico et al, 2002;Shibolet et al, 2002;Yeo et al, 2002). The use of the proposed predictive model may aid the identification of high-risk patients who stand to benefit most from the antiviral, which could in turn be administered in a most cost-effective manner.…”

Section: Discussionmentioning

confidence: 99%

“…The incidence of HBV reactivation in hepatitis B surface antigen (HBsAg) seropositive cancer patients undergoing cytotoxic chemotherapy has been reported to be 20% or higher (Lok et al, 1991;Nokamura et al, 1996;Kumagai et al, 1997;Markovic et al, 1999;Yeo et al, 2000a). No preventive measures have been proven to prevent or reduce the incidence of HBV reactivation, although more recent reports have suggested that the prophylactic use of the antiviral agent lamivudine, prior to the start of chemotherapy, may reduce the occurrence of the condition (Rossi et al, 2001;Liao et al, 2002;Lim et al, 2002;Persico et al, 2002;Shibolet et al, 2002;Yeo et al, 2002). There has also been concern about the emergence of viral mutant as a result of lamivudine therapy, and, to date, limited data are available on the clinical impact of these mutants in immunosuppressed subjects.…”

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confidence: 99%

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Comprehensive analysis of risk factors associating with Hepatitis B virus (HBV) reactivation in cancer patients undergoing cytotoxic chemotherapy

et al. 2004

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For cancer patients with chronic hepatitis B virus (HBV) infection, who receive cytotoxic chemotherapy, HBV reactivation is a welldescribed complication, which may result in varying degrees of liver damage. Several clinical features and the pre-chemotherapy HBV viral load have been suggested to be associated with an increased risk of developing the condition: (1) to assess the clinical and virological factors in a comprehensive manner and thereby identify those that are associated with the development of HBV reactivation; (2) to develop a predictive model to quantify the risk of HBV reactivation. In all, 138 consecutive cancer patients who were HBV carriers and undergoing chemotherapy were studied, of which 128 patients had sera available for real-time PCR HBV DNA measurement. They were followed up throughout their course of chemotherapy and the HBV reactivation rate was determined. The clinical and virological features between those who did and did not develop viral reactivation were compared. These included age, sex, baseline liver function tests, HBeAg status and viral load (HBV DNA) prior to the chemotherapy, and the use of specific cytotoxic agents. In all, 36 (26%) developed HBV reactivation. Multivariate analysis revealed pre-chemotherapy HBV DNA level, the use of steroids and a diagnosis of lymphoma or breast cancer to be significant factors. Based on real-time HBV DNA PCR assay, detectable baseline HBV DNA prior to the administration of cytotoxic chemotherapy, the use of steroids and a diagnosis of lymphoma or breast cancer are predictive factors for the development of HBV reactivation. A predictive model was developed from the current data, based on a logistic regression method.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Comprehensive analysis of risk factors associating with Hepatitis B virus (HBV) reactivation in cancer patients undergoing cytotoxic chemotherapy

et al. 2004

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“…This will lead to the development of lamivudine resistance caused by point mutations, with substitution of either valine or isoleucine for the amino acid position 204 methionine (rtM204V or rtM204I, respectively) in the HBV DNA polymerase gene (tyrosinemethionine-aspartate-aspartate [YMDD] motif) [67]. Its risk increases as the therapy is prolonged, reaching a level of 67% after 4 years in nonimmunocompromised patients Jang et al 88 Lim et al 127 Yeo et al 119 Lee et al 118 Idilman et al 117 Yeo et al 116 Leaw et al 115 Ozguroglu et al 114 Lau et al 85 Persico et al 113 Shibolet et al 112 Dai et al 111 Nagamatue et al 58 0.001 0.01 0.1 1 10 100 1000…”

Section: Preemptive Use Of Nucleoside Analoguesmentioning

confidence: 99%

Hepatitis B reactivation after chemotherapy: two decades of clinical research

Lau

2008

Hepatol Int

102

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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. How important is the problem?Over the past 20 years of clinical practice at Queen Mary Hospital, we have seen a lot of progress in the management of hepatitis due to HBV reactivation in hepatitis B surface antigen carriers [1][2][3][4][5]. In the past, we saw patients who died of fulminant hepatic failure after being administered a few courses of cytotoxic therapy to treat their life-threatening lymphoma [6][7][8][9] and breast cancer [10][11][12] if they were also hepatitis B surface antigen positive. At that time, the literature report of this important clinical issue was scanty. The first report in the field was published by Wand et al. [13] who studied the effects of antitumor chemotherapeutic agents on hepatitis antigen (HBAg) and antibody (HBAb) in 25 patients with myeloproliferative and in 60 patients with lymphoproliferative disorders. This elegant study was performed at the time when only antigen and antibody associated with viral hepatitis could be semiquantified [14]. In those patients who had HBAg at the time of initiation of chemotherapy, bone marrow suppression by chemotherapeutic agents was associated with a marked increase in HBAg titer, which was then followed by hepatocellular damage, as manifested by an elevation in serum transaminase enzymes [13]. Since then, this important observation was further confirmed in other studies [8,15,16], with the rate of HBV reactivation ranging from 19% to 48%. Among them, one-quarter to half would be complicated, with severe hepatitis...

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“…[1][2][3] These reactivations have been observed, especially in hepatitis B surface antigen (HBsAg)-positive subjects 4 and they occur in 20%-50% of cases, with a mortality rate of 10%-40%. Consequently, lamivudine prophylaxis is strongly recommended in HBsAg-positive subjects receiving chemotherapy or immunosuppressive therapy, [5][6][7] although there are no clear guidelines for HBsAg-negative subjects.…”

Section: Introductionmentioning

confidence: 99%

HBV reactivation with fatal fulminating hepatitis during rituximab treatment in a subject negative for HBsAg and positive for HBsAb and HBcAb

Sarrecchia

Cappelli

Aiello

2005

Journal of Infection and Chemotherapy

110

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A 51-year-old man who was hepatitis B surface antigen (HBsAg)-negative and positive for anti-hepatitis B surface antigen (anti-HBs) and anti-hepatitis B core antigen (anti-HBc), during rituximab therapy for chronic Lymphocytic leukemia, developed reactivation of hepatitis B virus (HBV) infection with hepatitis that proceeded towards hepatic failure and death in spite of lamivudine therapy. HBsAg remained persistently negative, notwithstanding a high HBV-DNA titer. Our observation, following other cases of fatal reactivation of HBV infection in patients receiving rituximab, suggests that, in all patients with previous markers of HBV infection, lamivudine prophylaxis should be considered during rituximab therapy.

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Lamivudine therapy for prevention of immunosuppressive-induced hepatitis B virus reactivation in hepatitis B surface antigen carriers

Cited by 143 publications

References 39 publications

Comprehensive analysis of risk factors associating with Hepatitis B virus (HBV) reactivation in cancer patients undergoing cytotoxic chemotherapy

Comprehensive analysis of risk factors associating with Hepatitis B virus (HBV) reactivation in cancer patients undergoing cytotoxic chemotherapy

Hepatitis B reactivation after chemotherapy: two decades of clinical research

HBV reactivation with fatal fulminating hepatitis during rituximab treatment in a subject negative for HBsAg and positive for HBsAb and HBcAb

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