Hepatitis B virus carriers in the treatment of malignant lymphoma: An epidemiological study in Japan

Kumagai, Kyoya; Takagi, Toshiyuki; Nakamura, Shinobu; Sawada, Umihiko; Kura, Yurie; Kodama, Fumio; Shimano, Shunichi; Kudoh, Ichidai; Nakamura, Hajime; Sawada, Kenichi; Ohnoshi, Taisuke

doi:10.1093/annonc/8.suppl_1.s107

Cited by 109 publications

(115 citation statements)

References 16 publications

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“…The condition is manifested with abnormal liver function tests that show a hepatitic picture, and it is confirmed by raised levels of serum HBV DNA. The clinical spectrum ranges from asymptomatic hepatitis to fatal hepatic failure (Galbraith et al, 1975;Hoofnagle et al, 1982;Lok et al, 1991;Nokamura et al, 1996;Kumagai et al, 1997;Markovic et al, 1999;Yeo et al, 2000a). However, even in its mildest form with spontaneous recovery, a patient's prognosis from cancer may still be impaired from the disruption in chemotherapeutic administration with treatment delay, or premature termination of the anticancer therapy.…”

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confidence: 99%

“…However, even in its mildest form with spontaneous recovery, a patient's prognosis from cancer may still be impaired from the disruption in chemotherapeutic administration with treatment delay, or premature termination of the anticancer therapy. 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).…”

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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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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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“…After the withdrawal of chemotherapy, partial recovery of cytotoxic T-cell-mediated immune response causes rapid destruction of the infected hepatocytes [20]. This complication has been well known for over 25 years and poses a major risk for these patients, with varying morbidity and mortality rates [1,2,17,[28][29][30][31][32]. The severity of the subsequent liver damage cannot be predicted and may range from slight elevation of aminotransferases to fatal fulminant hepatitis [13,20,33].…”

Section: Reactivation Of Hepatitis B In Patients With Chronicmentioning

confidence: 99%

“…The liver damage that is caused is characterized by varying degrees of severity, including jaundice and fatal hepatic failure in 10-63% and 4-71% of the cases, respectively [1,[4][5][6][7]. It may also cause delays or modifications of therapy or even its cessation [4,8].…”

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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

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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.

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Frequency of hepatitis B virus reactivation in cancer patients undergoing cytotoxic chemotherapy: A prospective study of 626 patients with identification of risk factors

et al. 2000

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Hepatitis B virus (HBV) reactivation is a well-described complication in cancer patients who receive cytotoxic chemotherapy and may result in varying degrees of liver damage. As chemotherapy is used increasingly in cancer patients, HBV reactivation during cytotoxic treatment may become a more common problem. In lymphoma patients, the incidence of chronic HBV infection has been reported to be 26%, of whom 47% developed HBV reactivation during chemotherapy. However, corresponding data for patients with other malignancies undergoing cytotoxic chemotherapy are not known. In this prospective study, hepatitis B surface antigen (HBsAg) was determined in 626 consecutive cancer patients who received cytotoxic chemotherapy over a 12-month period. Seventy-eight patients (12%) were found to be HBsAg positive. Thirty-four (44%) developed raised alanine transaminase during their course of chemotherapy. In these 34 patients, hepatitis was attributed to HBV reactivation in 15 patients (44%), chronic active HBV infection in 1 patient (3%), hepatitis C infection in 1 patient (3%), malignant hepatic infiltration in 2 patients (6%), and the use of hepatotoxic chemotherapeutic agents in 11 patients (32%). The causes of hepatitis were unknown in 4 patients (12%). HBV reactivation was more likely to develop in patients who were male, younger age, HBeAg seropositive, and those with lymphoma. Presence of malignant hepatic infiltration, baseline pre-treatment alanine transaminase, total bilirubin, and HBV DNA levels did not correlate with the development of HBV reactivation. Of the 15 patients who developed HBV reactivation, antiviral therapy with lamivudine was available and used in 9. There was no HBV-related mortality during chemotherapy. It is concluded that in patients with chronic HBV infection under chemotherapy, HBV reactivation occurs in nearly 20% of them and accounts for 44% of hepatitis cases. The risk factors identified include male sex, younger age, HBeAg seropositive, and the diagnosis of lymphoma. In HBV endemic areas, patients with risk factors for HBV reactivation should be identified prior to receiving cytotoxic treatment and monitored closely. The potential benefit of lamivudine requires further confirmation.

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Hepatitis B virus carriers in the treatment of malignant lymphoma: An epidemiological study in Japan

Cited by 109 publications

References 16 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

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

Frequency of hepatitis B virus reactivation in cancer patients undergoing cytotoxic chemotherapy: A prospective study of 626 patients with identification of risk factors

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