Fulminant Hepatic Failure in Leukaemia and Choriocarcinoma Related to Withdrawal of Cytotoxic Drug Therapy

Galbraith, R M; Williams, Roger; Eddleston, A L W F; Zuckerman, A. J.; Bagshawe, K. D.

doi:10.1016/s0140-6736(75)90897-1

Cited by 236 publications

(120 citation statements)

References 3 publications

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“…Apart from steroids and anthracyclines, other drugs that have been reported included vincristine, bleomycin, etoposide, methotrexate, actinomycin D, mercaptopurine, azauridine, chlorambucil, cytosine arabinoside, leucovorin, cisplatin and gemcitabine (Galbraith et al, 1975;Hoofnagle et al, 1982;Thung et al, 1985;Bird et al, 1989;Lau et al, 1989;Liang et al, 1990;Pinto et al, 1990;Lok et al, 1991;Soh et al, 1992;Nokamura et al, 1996;Wong et al, 1996;Yeo et al, 2000a). In the present study, it is interesting to find that the use of steroids was an associated risk factor on multivariate analysis.…”

Section: Discussionmentioning

confidence: 54%

“…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%

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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: 54%

mentioning

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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“…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, hepatic failure, and even death [1][2][3][4][5][6][17][18][19][20].…”

Section: How Important Is the Problem?mentioning

confidence: 79%

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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“…It is considered that chemotherapy--induced immunosupression may be faborable to the spread of HBV infection among hepatocytes, and that a host's cellular immune response to viral antigen may rebound when the therapy is stopped. In some of these patients, it may result in massive hepatic necrosis (Galbraith et al 1975 ;Wand 1975 ;Hoofnagle et al 1982). In the same way, a pronounced rebound of immune response to HBV replication with rapid tapering or abrupt discontinuance of immunosupressants such as steroids may precipitate hepatic decompensation in HBsAg-positive patients with chronic liver diseases like our patient (Case No.…”

Section: Discussionmentioning

confidence: 99%

Severe acute exacerbation in chronic hepatitis B virus infection in Sendai, Japan.

Kanno

Suzuki²,

Miyazaki³

et al. 1988

Tohoku J. Exp. Med.

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In order to examine the clinical features of severe acute exacerbation in chronic hepatitis B virus (HBV) infection, 297 hepatitis B surface antigen (HBsAg) carriers were followed for 35+22 months (mean+s.D.) in Tohoku University Hospital from 1976 to 1987. Of these, 10 experienced severe acute exacerbation with hepatic decompensation. All of these patients had intense subjective symptoms related to the hepatitis. They were all icteric and 8 had ascites. Three developed to fulminant hepatic failure, eventually died. Histology after the exacerbation showed severe hepatic damage such as massive hepatic necrosis and bridging hepatic necrosis in a half of them. Six cases were suspected to result from spontaneous reactivation and 2 from drug-induced reactivation of chronic HBV infection, and the other 2 from superinfection with non-A, non-B hepatitis agent (s). These results suggest that the reactivation of chronic HBV infection is an important factor of severe acute exacerbations in chronic HBV infection in Japan.severe acute exacerbation ; HBsAg carrier ; reactivation of chronic HBV infection Patients with chronic type B hepatitis positive for hepatitis B e antigen (HBeAg) are considered to experience frequent acute exacerbations (Perrilo et al. 1984;Liaw et al. 1987). However, the exacerbations occasionally occur in hepatitis B surface antigen (HBsAg) carriers negative for HBeAg (Liaw et al. 1987). Such exacerbations are considered to be induced by the spontaneous reactivation of chronic hepatitis B virus (HBV) infection and superinfections with hepatitis A virus (HAY) (Zachoval et al. 1983;Davis et al. 1984b), non-A, non-B (NANB) hepatitis agent (s) (Papaevangelou et al. 1984) and hepatitis delta

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Fulminant Hepatic Failure in Leukaemia and Choriocarcinoma Related to Withdrawal of Cytotoxic Drug Therapy

Cited by 236 publications

References 3 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

Severe acute exacerbation in chronic hepatitis B virus infection in Sendai, Japan.

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