RESUMO
We describe 5 cases of fulminant hepatitis caused by the HBV infection in patients with haematological diseases, mostly malignancies (ALL, lymphoma, aplastic anemia, AML) following intensive chemotherapy. Infection was confirmed by serological examination (HBsAg positivity) and by electron microscopy (viral particles). After termination of chemotherapy fulminant hepatitis developed with hepatic failure and very high levels of AST and ALT. Autopsy revealed massive necrosis without signs of regeneration. We suggest that immunosuppressive therapy increases the risk of severe infection of hepatocytes with HBV and subsequent withdrawal of chemotherapy causes "immunological rebound" leading to massive necrosis.
Assuntos
Anemia Aplástica/complicações , Hepatite B/etiologia , Linfoma/complicações , Anemia Aplástica/tratamento farmacológico , Anemia Aplástica/patologia , Feminino , Hepatite B/patologia , Hepatite B/virologia , Hepatite Crônica/etiologia , Hepatite Crônica/patologia , Hepatite Crônica/virologia , Humanos , Linfoma/tratamento farmacológico , Linfoma/patologia , Masculino , Leucemia-Linfoma Linfoblástico de Células Precursoras/complicações , Leucemia-Linfoma Linfoblástico de Células Precursoras/tratamento farmacológico , Leucemia-Linfoma Linfoblástico de Células Precursoras/patologiaRESUMO
In HBV related hepatitis it is generally accepted that the liver injury is mediated by an immune response to the virus, since HBV is not directly cytopathic. The first step in cytotoxic T lymphocyte mediated immune reaction in HBV infected mice is the induction of apoptosis. The role of BCL-2, p53 and PCNA (as the main regulators of cell cycle homeostasis) in this process has not been studied. The aim of this pilot study is to estimate immunohistochemically the expression of the BCL-2, p53 and PCNA in a group of HBV infected patients at various stages of the disease. Formalin fixed, paraffin embedded liver biopsies from 5 patients with HBsAG positivity in their serum were used for immunohistochemical study of the expression of BCL-2, PCNA (PC10) and P53 (DO1clone). As the chromogen we used both the DAB and AEC. The results were co-related with the 3 liver biopsies as controls. In the hepatocytes of the all cases (including controls) we did not found any positivity of BCL-2, p53 and PCNA. However the majority of the lymphocytes present in the liver of some cases of HBV infected patients were strongly BCL-2 positive. This preliminary results of very small group of patients could indicate that hepatocytes in the HBV infection are in the quiescent stage as in the controls and that the cell cycle regulation during infection could be controlled by other genes such as bax, bcl-Xs, FAS etc., but further studies are required.
