1/78. Transient hypoplastic anemia caused by primary human parvovirus B19 infection in a previously untreated patient with hemophilia transfused with a plasma-derived, monoclonal antibody-purified factor viii concentrate.BACKGROUND: Modern plasma-derived clotting factor concentrates are produced using various virus-inactivation protocols and are assumed to be safer than they were previously with regard to the risk for transmitting viral infections such as human immunodeficiency virus, hepatitis B, and hepatitis c. The risks from viruses that are relatively resistant to the current inactivation procedures remain uncertain. PATIENT: A 7-year-old with mild hemophilia a who had not been previously infused with any blood products was treated with a plasma-derived, monoclonal antibody-purified factor viii concentrate to cover orthopedic surgery after traumatic fracture of his left arm. RESULTS: A typical primary human parvovirus (HPV)-B19 infection was observed associated with transient hypoplastic anemia. retrospective studies including serologic examination and polymerase chain reaction analysis confirmed that the HPV-B19 infection was transmitted by the factor viii concentrate. CONCLUSIONS: Clotting factor concentrates for the treatment of hemophilia retain a risk for HPV-B19 contamination. HPV-B19 viral infection might induce hypoplastic anemia in these patients, particularly during enhanced hemopoiesis after acute blood loss.- - - - - - - - - - ranking = 1keywords = hepatitis (Clic here for more details about this article) |
2/78. Successful cytokine treatment of aplastic anemia following living-related orthotopic liver transplantation for non-A, non-B, non-C hepatitis.The relationship between aplastic anemia and viral hepatitis is well recognized, and such patients usually have a high mortality. We successfully treated a case of aplastic anemia following living-related orthotopic liver transplantation (LROLT) for non-A, non-B, non-C hepatitis. A 2-yr-old boy with fulminant hepatic failure from non-A, non-B, non-C hepatitis received LROLT. Before transplantation, he had pancytopenia which was probably hepatitis associated, and viral suppression was suspected after bone marrow (BM) biopsy. After the transplantation, he developed progressive pancytopenia and a diagnosis of aplastic anemia was made via BM biopsy. With immunosuppressant agents (cyclosporine, methylprednisolone), cytokine therapy (granulocyte-colony stimulating factor (G-CSF), macrophage-colony stimulating factor (M-CSF), recombinant human erythropoietin (rhEPO)) was effectual and the patient recovered from pancytopenia. He was discharged from the hospital 57 d after the liver transplantation and remains well 1 yr after LROLT. Combined cytokine therapy with high doses of G-CSF, M-CSF and rhEPO appeared to be effective in the treatment of aplastic anemia following liver transplantation for non-A, non-B, non-C hepatitis. Since M-CSF activates macrophages, it may have contributed to the graft rejection. Careful consideration should be given to the use of high-dose M-CSF in liver transplant patients.- - - - - - - - - - ranking = 4.5keywords = hepatitis (Clic here for more details about this article) |
3/78. Hepatitis G virus infection as a possible causative agent of community-acquired hepatitis and associated aplastic anaemia.Aplastic anaemia complicating hepatitis is a rare but well-documented phenomenon; however in many patients the cause remains unknown. We present a 24-year-old man with a well-defined community-acquired hepatitis, probably due to hepatitis G virus (HGV), who developed severe aplastic anaemia. In this case, the absence of other agents likely to cause the clinical manifestations, and the detection of HGV rna at the time of illness, clearly point to this agent as being responsible for both the hepatitis and the aplastic anaemia. Further studies in serial serum samples and meticulous evaluation of the disorders associated with the infection will be needed to prove or dispute a causal association of HGV and aplastic anaemia.- - - - - - - - - - ranking = 4keywords = hepatitis (Clic here for more details about this article) |
4/78. Syngeneic peripheral blood stem cell transplantation with brief immunosuppression for severe aplastic anemia.We report the cases of two severe aplastic anemia (SAA) patients who were successfully treated with syngeneic peripheral blood stem cell transplantation (PBSCT) using immunosuppression without high-dose chemotherapy or irradiation for conditioning. A 21-year-old woman with SAA of 6 years duration had been transfused heavily before transplantation and had developed refractory thrombocytopenia, chronic hepatitis and secondary hematochromatosis. Syngeneic PBSCT with immunosuppression using ATG, methylprednisolone, and cyclosporin-A was eventually performed without high-dose chemotherapy in September 1997. The second syngeneic PBSCT with the same immunosuppression was successfully performed in a 35-year-old male patient who had had SAA for 3 months in November 1998. Haemopoietic engraftment was rapid and sustained. There was no infection or mucositis during the syngeneic PBSCT. The patients are currently 9 to 22 months post-PBSCT without rejection. Our experience suggests that syngeneic PBSCT with brief immunosuppression is an effective alternative to pretransplant high-dose chemotherapy conditioning for SAA patients having syngeneic transplantation. bone marrow transplantation (2000) 25, 337-339.- - - - - - - - - - ranking = 0.5keywords = hepatitis (Clic here for more details about this article) |
5/78. Indirect evidence of TTV replication in bone marrow cells, but not in hepatocytes, of a subacute hepatitis/aplastic anemia patient.The presence of a new dna virus (TTV) has been reported in sera from patients with posttransfusion hepatitis of unknown etiology. The precise replication site of TTV, however, has not been established. In this study, the presence of TTV in liver autopsy material, and in bone marrow biopsy and autopsy samples taken from a subacute hepatitis/aplastic anemia patient was determined by PCR and Southern blot analyses. Liver cells were found to contain only TTV dna and not mRNA. Bone marrow material, especially that taken at biopsy, contained high levels of TTV dna. It is suggested that the TTV replication site was in the bone marrow rather than in the liver, and that TTV infection was the cause of this patient's aplastic anemia. The precise etiological association of TTV with hepatitis remains to be established.- - - - - - - - - - ranking = 3.5keywords = hepatitis (Clic here for more details about this article) |
6/78. Intra-hepatic haematoma complicating transjugular intra-hepatic portosystemic shunt for budd-chiari syndrome associated with anti-phospholipid antibodies, aplastic anaemia and chronic hepatitis c.Portal venous decompression with transjugular intra-hepatic portosystemic shunt (TIPS) is a new approach in the treatment of budd-chiari syndrome. We report on a 31-year-old female with budd-chiari syndrome due to anti-phospholipid antibodies with compression of the inferior vena cava treated with TIPS and stenting of the inferior vena cava. TIPS was complicated by massive intra-hepatic haematoma which was managed conservatively. Treatment options and pathogenic mechanisms of budd-chiari syndrome under the rare coincidence of aplastic anaemia and anti-phospholipid syndrome are discussed. TIPS may be considered for venous decompression in budd-chiari syndrome, but physicians should be aware of potential TIPS' complications in these patients.- - - - - - - - - - ranking = 2keywords = hepatitis (Clic here for more details about this article) |
7/78. Hepatitis-associated aplastic anemia and transfusion-transmitted virus infection.A 17-year-old man was admitted to our hospital because of severe acute hepatitis. Serologic studies were negative for A, B, C and G hepatitis viruses. Later, he was found to be positive for transfusion-transmitted virus (TTV) dna. He was discharged after normalization of liver function tests. Four months after the onset of hepatitis, he was re-admitted because of pancytopenia. Bone marrow findings were consistent with aplastic anemia. The anemia responded to steroid therapy. In this case, TTV was probably involved in the development of aplastic anemia.- - - - - - - - - - ranking = 1.5keywords = hepatitis (Clic here for more details about this article) |
8/78. Prolonged bone marrow failure with monosomy 7 after engraftment failure following bone marrow transplantation.A patient with acute myelogenous leukemia developed prolonged bone marrow failure along with the monosomy 7 chromosome abnormality. The patient had undergone bone marrow transplantation with CD34 selection following induction failure. However, she then suffered engraftment failure and long-term pancytopenia. Her white blood cell count gradually increased with supportive therapy including granulocyte colony-stimulating factor (G-CSF), and chromosomal analysis of bone marrow cells revealed an abnormal karyotype. Thirty months after the bone marrow transplantation we observed monosomy 7 together with the existing chromosomal abnormality in the patient's bone marrow cells. It has been reported that some patients with idiopathic and posthepatitis aplastic anemia develop clonal disorders such as myelodysplastic syndrome/acute myelogenous leukemia with monosomy 7. The findings in our case suggest that the appearance of monosomy 7 in patients with aplastic anemia may be caused by prolonged low-level hematopoiesis, with or without G-CSF stimulation.- - - - - - - - - - ranking = 0.5keywords = hepatitis (Clic here for more details about this article) |
9/78. Successful bone marrow transplantation for severe aplastic anemia following orthotopic liver transplantation: long-term follow-up and outcome.Severe aplastic anemia (SAA) is well described in children following liver transplantation for fulminant hepatic failure (FHF) secondary to non-A, non-B, non-C hepatitis, and is associated with a high mortality rate. Successful immunosuppressive treatment of SAA following liver transplantation has been reported, but death from infectious complications is not uncommon. We report the 8-year follow-up of a 3.5-year-old boy who underwent successful HLA-identical sibling donor bone marrow transplant for SAA 7 months following orthotopic liver transplant for non-A, non-B, non-C hepatitis. His post-bone marrow transplantation course was uneventful with no evidence of liver toxicity. Eight months following BMT he developed renal cell carcinoma metastatic to lymph nodes which was treated surgically. Six years following BMT he developed a mucoepidermoid carcinoma of the parotid gland also treated surgically. Despite these malignancies, he is currently well 8 years following liver and bone marrow transplantation, without signs of GVHD, growth failure or liver graft rejection. This is the first report of long-term follow-up of bone marrow transplantation for SAA following liver transplantation. The occurrence of two subsequent malignancies in this child underscores the need for close follow-up of future similar cases.- - - - - - - - - - ranking = 1keywords = hepatitis (Clic here for more details about this article) |
10/78. Reactivation of precore variant hepatitis b virus in a child with severe aplastic anaemia.Reactivation of hepatitis B e antigen (HBeAg) negative chronic hepatitis b virus (HBV) infection due to selection of precore variant virus is an uncommon complication of previous hepatitis B infection, and virtually unrecognised in children and adolescents. A child who had received treatment with methylprednisolone and antilymphocyte globulin for severe aplastic anaemia developed high levels of detectable HBV dna associated with hepatitis B e antibody (anti-HBe) positivity. HBV dna was extracted, amplified and the core and precore regions sequenced from 2 samples. A mixture of wild-type and the precore variants A(1896) and A(1899) was detected in both samples, with the wild-type predominating in the second sample. Reinfection was excluded by phylogenetic analysis using Phylip and the neighbour-joining method. Precore variant hepatitis b virus can be transmitted to children as a primary infection, and it is important that aggressive liver disease, particularly in the presence of the anti-HBe phenotype, be investigated. Further studies are needed to determine the frequency of these variants.- - - - - - - - - - ranking = 4keywords = hepatitis (Clic here for more details about this article) |
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