Hepatitis B associated liver failure following bone marrow transplantation

Caselitz, M; Link, H.; Hein, R. H.; Maschek, H.; Böker, K. H. W.; Poliwoda, H.; Manns, Michael P.

doi:10.1016/s0168-8278(97)80363-7

Cited by 54 publications

(24 citation statements)

References 12 publications

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“…14 Hepatic complications related to HBV infection after HCT are primarily associated with HBV reactivation. 2,5,10,11,13,[15][16][17] The underlying pathogenesis of HBV reactivation is likely to be related to the intensive chemotherapy with or without total-body irradiation (TBI) required to ablate the recipients' marrow. 18 Prospective serologic testing of patients with chronic HBV infection who have HBV reactivation after chemotherapy showed that immunosuppression enhances viral replication.…”

Section: Introductionmentioning

confidence: 99%

High hepatitis B virus (HBV) DNA viral load as the most important risk factor for HBV reactivation in patients positive for HBV surface antigen undergoing autologous hematopoietic cell transplantation

Lau

Leung

Fong

et al. 2002

Blood

209

143

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Section: Introductionmentioning

confidence: 99%

High hepatitis B virus (HBV) DNA viral load as the most important risk factor for HBV reactivation in patients positive for HBV surface antigen undergoing autologous hematopoietic cell transplantation

Lau

Leung

Fong

et al. 2002

Blood

209

143

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“…10,15,18,21,25 In the setting of hematopoietic stem cell transplantation (HSCT) for various hematological and oncological conditions, HBV reactivation has been reported in over 50% of patients. [26][27][28] This is related to the intense chemotherapy with or without total body irradiation, and the coexistence of acute graft-versus-host disease. 28 Although the frequency of viral reactivation among HBsAg-positive patients with cancer would be expected to be the same irrespective of geographical area, the prevalence of HBV infection varies between different populations from 10% to 25% in endemic areas to less than 1% in others.…”

mentioning

confidence: 99%

Diagnosis, prevention and management of hepatitis B virus reactivation during anticancer therapy

2006

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It is estimated conservatively that more than one third of the world's population has been infected with the hepatitis B virus (HBV) and that there are 350 million people with chronic infection, 75% of whom live in Southeast Asia and the Western Pacific regions. [1][2][3] Reactivation of HBV infection is now a well-recognized complication in infected patients who undergo cytotoxic chemotherapy for cancer. The condition ranges from asymptomatic self-limiting anicteric hepatitis to severe, potentially fatal progressive decompensated hepatitis. With the increasing use of potent cytotoxic chemotherapy, reactivation of hepatitis B in endemic regions is becoming a common clinical problem. This adversely affects advances made in various forms of cancer therapy. In this review, we consider the diagnosis, prevention, and management of HBV reactivation in association with chemotherapy and hematopoietic stem cell transplantation, particularly in light of the availability of effective prophylactic antiviral therapy.Reactivation of HBV was first described by Wands et al., 4 who in 1975 reported the condition in 20 patients with lympho-and myeloproliferative disorders. Most of the cases reported since were similar in patients with hematological malignancies-in particular, lymphomas. [4][5][6][7][8][9][10][11][12][13][14][15][16] The skewed observations may be due to the fact that these patients are often subjected to intense myelosuppressive treatment regimens, the malignancies per se are often associated with an immunocompromised state, and the patients have been consistently reported to have a higher rate of hepatitis B surface antigen (HBsAg) seropositivity than the normal population. 9,[17][18][19] Over the past decade, HBV reactivation has been increasingly observed in patients with solid tumors. [18][19][20][21][22] In patients with hepatocellular carcinoma (85% of whom have chronic HBV infection in Southern China 3,23 ), hepatitis following systemic chemotherapy has been reported in 60% 20,24 ; this is mostly attributed to HBV reactivation, which has a 30% mortality rate. 20 In other cancer subpopulations, the incidence of HBV reactivation ranges between 25% and 40%. 10,15,18,21,25 In the setting of hematopoietic stem cell transplantation (HSCT) for various hematological and oncological conditions, HBV reactivation has been reported in over 50% of patients. [26][27][28] This is related to the intense chemotherapy with or without total body irradiation, and the coexistence of acute graft-versus-host disease. 28 Although the frequency of viral reactivation among HBsAg-positive patients with cancer would be expected to be the same irrespective of geographical area, the prevalence of HBV infection varies between different populations from 10% to 25% in endemic areas to less than 1% in others. 3,10,29 As a result, there would be proportional difference in the incidence of viral reactivation in a given population. Definitions and DiagnosisIn early reports, the diagnosis of HBV reactivation was based on HBsAg and hepatitis B ...

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“…[1][2][3] In these cases, hepatitis has occasionally progressed to the fulminant stage and it is thought that this was induced by reactivation of HBV in the recipient's liver cells. The virus begins to proliferate during immunosuppression after BMT and then active hepatitis develops depending on the recovery of the immune response when doses of immunosuppressant are reduced or discontinued.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3] However, hepatitis occurring in patients who had been positive for anti-hepatitis B surface antibody (HBsAb) before BMT is rarely reported. [4][5][6] We report here lethal hepatic failure that developed in an immunosuppressed patient after allo-BMT due to reactivation of latent hepatitis B virus (HBV) despite having HBsAb and no virus DNA detected in the serum before transplantation.…”

mentioning

confidence: 99%

Fulminant hepatitis B following bone marrow transplantation in an HBsAg-negative, HBsAb-positive recipient; reactivation of dormant virus during the immunosuppressive period

Iwai

Tashima

Itoh

et al. 2000

Bone Marrow Transplant

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Summary:It is widely accepted that seroconversion of HBsAg to HBsAb indicates clearance of hepatitis B virus. We describe a 50-year-old man with chronic myelocytic leukemia who developed lethal hepatitis B 22 months after allo-BMT. He had been negative for HBsAg and positive for HBsAb before BMT. Hepatitis B virus latently existing in the liver cells before BMT proliferated during the immunosuppressed period causing fatal hepatitis. Recipients with positive HBsAb should be considered to have the potential for active hepatitis B to emerge after BMT. Bone Marrow Transplantation (2000) 25, 105-108. Keywords: bone marrow transplantation; hepatitis B; HBsAg-negative The risk of hepatitis B caused in patients positive for hepatitis B surface antigen (HBsAg) by reactivation of the virus after bone marrow transplantation (BMT) has been well recognized. 1-3 However, hepatitis occurring in patients who had been positive for anti-hepatitis B surface antibody (HBsAb) before BMT is rarely reported. [4][5][6] We report here lethal hepatic failure that developed in an immunosuppressed patient after allo-BMT due to reactivation of latent hepatitis B virus (HBV) despite having HBsAb and no virus DNA detected in the serum before transplantation. MethodsEIA enzyme immunoassay kits AxSYM (Dinabot, Tokyo, Japan) were used for detection of HBsAg, HBsAb, anti-HBV core antibody (HBcAb), HBV e antigen (HBeAg) and anti-HBV e antibody (HBeAb). Serum HBV was measured by the branched DNA probe method using commercial Quantiplex HBV-DNA (Chiron, Emeryville, CA, USA). All procedures were performed according to the manufacturer's recommendations. Polymerase chain reaction (PCR) assays were performed as described previously. 7 Case reportA 50-year-old man consulted our hospital in April 1995 for leukocytosis that had been found on a regular checkup at his company and which was accompanied by abdominal fullness. He had splenomegaly 16 cm below the left costal margin and the peripheral blood showed a leukocytosis with basophilia. Bone marrow aspiration and biopsy revealed a hypercellular marrow with a very low G/E ratio and an increased percentage of blast cells, although the value remained under 30%, and myelofibrosis. The karyotype of all bone marrow cells examined was 46XY, t(9;22) (q34;q11). BCR-ABL fusion mRNA was also detected by the PCR method. He was diagnosed as having a chronic myelocytic leukemia in accelerated phase and was treated with hydroxyurea and interferon-␣. Because stable hematological remission was not obtained and his disease was considered to be very close to blast crisis, he underwent unrelated bone marrow transplantation from an HLA one locus mismatched 43-year-old female donor in April 1996. He was given buslfan 3.6 mg/kg over 4 days, cytarabin 50 mg/kg over 3 days, and cyclophosphamide 60 mg/kg over 3 days without total body irradiation as conditioning therapy. FK506 and short-term methotrexate were used for prophylaxis of acute GVHD. Engraftment was confirmed on day 13 by X-chromosomal examination (FISH). The level of...

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Hepatitis B associated liver failure following bone marrow transplantation

Cited by 54 publications

References 12 publications

High hepatitis B virus (HBV) DNA viral load as the most important risk factor for HBV reactivation in patients positive for HBV surface antigen undergoing autologous hematopoietic cell transplantation

High hepatitis B virus (HBV) DNA viral load as the most important risk factor for HBV reactivation in patients positive for HBV surface antigen undergoing autologous hematopoietic cell transplantation

Diagnosis, prevention and management of hepatitis B virus reactivation during anticancer therapy

Fulminant hepatitis B following bone marrow transplantation in an HBsAg-negative, HBsAb-positive recipient; reactivation of dormant virus during the immunosuppressive period

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