Lamivudine for the treatment of hepatitis B virus reactivation following chemotherapy for non‐Hodgkin's lymphoma

Liao, Chun-Ann; Lee, Chuan–Mo; Wu, Hong-Cheng; Wang, Ming-Chung; Lu, Sheng‐Nan; Eng, Hock‐Liew

doi:10.1046/j.1365-2141.2002.03239.x

Cited by 84 publications

(70 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…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.…”

mentioning

confidence: 99%

See 1 more Smart Citation

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

et al. 2004

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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

et al. 2004

View full text Add to dashboard Cite

show abstract

“…Also, not all patients could withstand percutaneous liver biopsy as they might have clotting derangement, especially those with hematological malignancy [83]. Another viral factor that has been investigated is hepatitis B e antigen (HBeAg) but the results are conflicting [6,10,58,89,[93][94][95]. This is probably related to the presence of the precore/core promoter HBV mutants (i.e., HBeAg-negative/hepatitis B e antigen-positive chronic hepatitis B infection) [96].…”

Section: Risk Factors Involved In Hbv Reactivationmentioning

confidence: 99%

“…As hepatitis due to HBV virological reactivation is associated or preceded by enhanced HBV viral replication during the immunosuppressive phase, the initiation of antiviral treatment such as lamivudine [102][103][104][105][106][107][108][109] and famciclovir [84,110] (Table 2). A meta-analysis of these 13 studies with 702 HBsAg-positive patients (237 treated with preemptive lamivudine and 465 untreated controls), showed that the incidence of hepatitis due to HBV reactivation was 3.3% in the treated group and 35.0% in the untreated control group (odds ratio [OR]: 0.083; 95% CI: 0.045-0.155, P \ 0.0001).…”

Section: Preemptive Use Of Nucleoside Analoguesmentioning

confidence: 99%

Hepatitis B reactivation after chemotherapy: two decades of clinical research

Lau

2008

Hepatol Int

102

View full text Add to dashboard Cite

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...

show abstract

“…Most cases of HBV reactivation occur after the first two or three chemotherapy cycles [7,18]. Lamivudine can suppress viral replication as early as 1 week after its commencement.…”

Section: Reactivation Of Hepatitis B In Patients With Chronicmentioning

confidence: 99%

Prevention of hepatitis B reactivation with lamivudine in hepatitis B virus carriers with hematologic malignancies treated with chemotherapy—A prospective case series

et al. 2005

View full text Add to dashboard Cite

Administration of immunosuppressive treatment in hepatitis B virus carriers with malignancies is associated with the risk of hepatitis B reactivation. This complication is more frequent in patients with hematologic malignancies because administration of corticosteroids, the mainstay of treatment of these patients, is an independent risk factor for hepatitis B reactivation. When lamivudine is given prior to chemotherapy, it prevents the viral replication during the immunosuppression period; therefore, it might reduce the risk of hepatitis B exacerbation. We performed a prospective study to assess the efficacy of prophylactic administration of lamivudine in this setting. Ten hepatitis B virus carriers with hematologic malignancies were included in this study; seven were HBsAg positive, and three had isolated antiHBc and detectable HBV-DNA levels. Nine patients were given corticosteroids after the administration of lamivudine. Lamivudine was given per os at a dose of 100 mg once daily. In four patients that had not been previously treated with chemotherapy, lamivudine was started 19 days (median) (range, 0-35 days) prior to the onset of chemotherapy. The administration of lamivudine has not stopped since in any of our patients. After a median follow-up of 15 months (range 6-38 months), no hepatitis B reactivation was observed. HBV-DNA levels were decreased in all 6 patients who had detectable HBV-DNA at baseline. Lamivudine was well tolerated. Chemotherapy regimens were administered as planned, and their effectiveness was not compromised by lamivudine. In conclusion, prophylactic administration of lamivudine should be considered as a means of reducing the frequency of hepatitis B reactivation in hepatitis B virus carriers with hematologic malignancies who are being treated with chemotherapy. Am.

show abstract

Lamivudine for the treatment of hepatitis B virus reactivation following chemotherapy for non‐Hodgkin's lymphoma

Cited by 84 publications

References 13 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

Prevention of hepatitis B reactivation with lamivudine in hepatitis B virus carriers with hematologic malignancies treated with chemotherapy—A prospective case series

Contact Info

Product

Resources

About