Long-term liver function of recipients with hepatitis G virus infection after bone marrow transplantation

Abstract

Summary:To clarify the role of hepatitis G virus (HGV) infection in liver dysfunction following allogeneic BMT, we examined cryopreserved serum samples from 33 patients who had a history of blood transfusions before BMT and whose serum samples had been stored periodically, before BMT, on day 100, and thereafter for the presence of HGV-RNA and hepatitis C virus (HCV)-RNA by reverse transcription polymerase chain reaction. Nineteen patients (58%) out of 33 were positive for HGV-RNA before BMT and 10 for HCV-RNA. All patients positive for HCV-RNA were also positive for HGV-RNA. Patients were divided into three groups according to their viral status before BMT; namely, the G؉C؉ group (n = 10), the G؉C؊ group (n = 9) and the G؊C؊ group (n = 14). Two patients in the G؊C؊ group became positive for HGV-RNA after BMT. One patient in the G؉C؊ group suffered an acute exacerbation of hepatitis, with GPT levels reaching over 1000 IU/l, 2 and 3 years after BMT, showing quite a different clinical course from those in the G؉C؊ group. Excluding these three patients, GPT levels of the patients in the G؉C؉ group were significantly higher after day 100 and remained higher than those of patients in the G؉C؊ and G؊C؊ groups for at least 4 years. There were no significant differences in post-transplant GPT levels between the G؉C؊ group and the G؊C؊ group at any time point. Of the seven patients followed-up for 5 to 10 years, three patients became HGV-RNA-negative, while four remained positive. In the absence of HCV co-infection, the behavior of GPT values post transplant in patients with HGV infection did not differ from those without HGV infection. With respect to the patient who was G؉C؊ and showed high values of GPT 2 and 3 years post transplant, we suspect that his liver dysfunction might have been caused by some unknown virus or etiology. Keywords: GBV-C; HGV; BMT; liver function Correspondence: A Maruta, Department of Hematology/Chemotherapy, Kanagawa Cancer Center, 1-1-2 Nakao, Asahi-ku, Yokohama 241-0815, Japan Received 6 November 1998; accepted 15 March 1999Two hepatitis-associated viruses, GB virus C (GBV-C) and hepatitis G virus (HGV), were identified in 1995 and in 1996. 1,2 These two viruses were found to show a 95% nucleotide homology, which was thought to indicate that they were isolates of the same virus, members of the Flaviviridae family.

Hepatitis C virus in long-term bone marrow transplant survivors

“…5 Other papers analyze the results of serological tests in BMT and immunocompromised patients. 10,15,[17][18][19][20][21][22][23] Toma´s et al 23 found in a retrospective study of 61 BMT patients who had hepatic pathology, 29 patients with chronic hepatitis C of whom seven constantly tested anti-HCV negative but PCR positive. The Seattle group recommends hepatitis C testing, including viral RNA analysis.…”

Viral Hepatitis: Manifestations and Management Strategy

“…34 The prevalence of HCV infection in patients with B-cell non-Hodgkin lymphoma and other lymphoproliferative disorders is between 8% and 32% and presents a significant management concern in these patients, 35 especially given the rare cases of liver failure that have been reported. 36,37 However, the reality is that hepatic dysfunction, clinical hepatitis flares, and fulminant hepatic failure are very uncommon events in HCV-infected patients who receive chemotherapy when compared to HBV-infected patients.…”

Rare viral infections in children receiving hemopoietic stem cell transplant

“…Reverse seroconversion of HBV is not a rare complication in autologous HSCT, 43 and in allogeneic HSCT recipients the risk seems to be higher during the tapering of the immunosuppressive therapy. 42 Moreover, in this setting, fulminant hepatitis due to HCV 44,45 or HBV 46 has been described. Therefore, even if infection with hepatotropic viruses does not represent a major contraindication for HSCT, 47 a careful follow-up is recommendable, especially during immunosuppression tapering.…”

“…48 Finally, as regards infections due to 'other' hepatitis viruses, no data are available on HAV acute hepatitis after HSCT, while infection with HGV has been reported in HSCT recipients. [49][50][51] The data available in the pediatric population do not support any pathogenic role after either chemotherapy 52 or HSCT. 41 …”