Cases reported "Hepatitis C"

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1/47. Decreased diversity of hepatitis c virus quasispecies during bone marrow transplantation.

    To elucidate the role of host immune status in the evolution and complexity of hepatitis c virus (HCV) quasispecies, three chronic HCV-infected patients who underwent bone marrow transplantation (BMT) were studied. The three transplanted patients' sera were sampled at pre-BMT, 3 months after BMT, and 12 months after BMT and the nucleotide diversity and substitution of the hypervariable region (HVR) of HCV quasispecies were analyzed. The nucleotide diversity was high at the pre-BMT period (28.2-43.4 x 10(-2) nucleotide difference/site). HVR of HCV quasispecies then became homogeneous in the first 3 months after BMT (0.11-6.40 x 10(-2) nucleotide difference/site). The nucleotide diversity of HVR at 12 months after BMT of all three patients was higher than that of 3 months after BMT but still lower than that of pre-BMT (2.09-6.40 x 10(-2) nucleotide difference/site). The analysis on nucleotide substitution rate showed a higher value between pre-BMT and 3 months after BMT (0.624-0.708 nucleotide difference/site per year) than that between 3 months and 12 months after BMT (0.072-0.127 nucleotide difference/site per year). HCV rna titer decreased when the host had a low white cell count and increased accordingly. It was concluded that the evolution of HVR of HCV quasispecies related to the immune status of the host during BMT: after immunosuppression, an initial increase of viral populations was followed by the emergence of a dominant strain while the quasispecies gradually recovered as the immunity of the host gained its competence.
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2/47. Fatal virus-associated hemophagocytic syndrome associated with coexistent chronic active hepatitis b and acute hepatitis c virus infection.

    A 28-year-old man was admitted to our department with intermittent fever, hepatosplenomegaly and pancytopenia. Liver parameters and serum ferritin were markedly elevated. Bone marrow biopsy showed hypocellularity, histiocytic hyperplasia, and hemophagocytosis consistent with a virus-associated hemophagocytic syndrome (VAHS). There was serological evidence of chronic active hepatitis b and acute hepatitis c virus infection. The patient died despite aggressive immunosuppressive and supportive treatment. autopsy revealed signs of acute viral hepatitis with cholestasis. histiocytes engaged in hemophagocytosis were observed in bone marrow and spleen. The condition was interpreted as VAHS associated with chronic active hepatitis b and acute hepatitis c virus infection. To our knowledge this is the first report of a hemophagocytic syndrome in that setting.
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3/47. hepatitis c virus, autoimmunity and lymphoproliferation.

    We summarize clinical, laboratory and pathologic details regarding a patient who presented with extrahepatic disease manifestations of hepatitis c virus (HCV) infection, including cryoglobulinemic leg ulcers due to cutaneous vasculitis, peripheral sensorimotor neuropathy, and recurrent pulmonary infiltrates. The patient had evidence for B-cell lymphoproliferation, diagnosed as extranodal lymphoma on initial (though not subsequent) bone marrow examination, retroperitoneal lymphadenopathy, and the presence of a Type II IgM6 monoclonal rheumatoid factor which became cryoprecipitable on complexing to IgG. Chronic hepatitis was mild on liver biopsy, though fibrotic changes developed over a three-year period of follow-up. She had consistently normal liver function tests, except for a brief rebound effect on discontinuing interferon-alpha, and preterminally. Symptoms were only partially responsive to trials of corticosteroids, cytotoxic agents, plasmapheresis and interferon, and the patient ultimately died at The Mount Sinai Hospital of sepsis. We review current information regarding the spectrum of extrahepatic HCV infection, including pathogenic factors relevant to its overlapping autoimmune, rheumatic and lymphoproliferative disease manifestations. The exact prevalence of these HCV-related syndromes among the 1% of the world population estimated to be infected by this virus remains to be delineated. Chronicity of infection, and lack of efficacy of currently available therapy in effecting sustained clearance of the virus from the host, have made this an important public health problem that is likely to increase in significance. Possible relationships to non-Hodgkin's lymphoma may present novel opportunities to delineate the basis for oncogenesis in HCV infection.
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4/47. Use of radiation therapy in posttransplant lymphoproliferative disorder (PTLD) after liver transplantation.

    Posttransplant lymphoproliferative disorder (PTLD) is a common and life-threatening complication of immunosuppression used to prevent rejection of solid organ and bone marrow transplants. There is no standardized treatment algorithm, but numerous management strategies are available. We describe a patient who developed a solitary lymphoproliferative lesion in the porta hepatis 9 months after orthotopic liver transplant. Following reduction in immunosuppression with no response, she was treated with involved field radiotherapy utilizing CT-based treatment planning. A partial radiographic response was obtained, and she has not developed disease in the engrafted liver or systemically. Based on the present case report, involved field radiotherapy seems to be a reasonable treatment option for patients with localized PTLD. Int. J. Cancer (Radiat. Oncol. Invest.) 90:104-109, 2000.
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5/47. Aplastic anemia after transplantation for non-A, non-B, non-C fulminant hepatic failure: case report and review of the literature.

    Aplastic anemia is a rare complication of liver transplantation (<1%). However, an increasing number of cases of aplastic anemia have been recently reported when liver transplantation is performed for non-A, non-B, non-C fulminant hepatic failure. The aim of this study is to reevaluate the importance and the incidence of aplastic anemia after liver transplantation for non-A, non-B, non-C fulminant hepatic failure, and to propose preventive measures, diagnostic and management guidelines to try to reduce the incidence, morbidity and mortality associated with this complication. In this report a case of aplastic anemia after liver transplantation for non-A, non-B, non-C fulminant hepatic failure is described. In addition, the pertinent literature on aplastic anemia after liver transplantation, since the first description of that complication in 1987, is reviewed. A 20-year-old woman developed aplastic anemia 14 weeks after liver transplantation for fulminant non-A, non-B, non-C hepatitis. After failure of G-CSF treatment, she was treated with intensive immunosuppression (FK 506, ATG, high-dose steroids). She is well 1 year post-transplantation, with normal liver tests and with bone marrow recovery. Through a medline literature search (1988-1999), we identified 30 additional cases of aplastic anemia following liver transplantation for non-A, non-B, non-C fulminant hepatic failure. Of all liver transplantations performed for that indication at five participating centers, the mean incidence of aplastic anemia was 23.2%. Mean age was 10 years (1.2-29) and the male/female ratio was 4.6. For treating aplastic anemia, different modalities were used: ATG ( n=12), ALG ( n=1), OKT 3 ( n=1), G-CSF ( n=6), a 6-HLA-compatible bone marrow transplantation ( n=3), and none ( n=12). The mortality rate remains high (39%), with infections and bleeding as the two most frequent causes of death. Based on this literature review, we conclude that aplastic anemia is a relatively common complication of liver transplantation for non-A, non-B, non-C fulminant hepatic failure in children and young adults. An unknown viral agent operating through immune-mediated mechanisms is probably responsible. The myelotoxic environment inherent to transplantation (e.g. azathioprine, trimethoprim) probably has a cumulative effect. Preventive measures (e.g. not using myelotoxic drugs) should be adopted in high-risk children and young adults transplanted for non-A, non-B, non-C fulminant hepatic failure. Early detection of bone marrow depression, a low threshold for performing a bone marrow biopsy, and prompt treatment are pivotal. Intensive standard supportive care with broad-spectrum antibiotics and anti-fungal agents is essential during phases of pancytopenia. Although spontaneous recovery has been described under maintenance immunosuppression, increased immunosuppression, in particular with ATG, may reverse the aplastic anemia and promote bone marrow recovery. In unresponsive patients, six-HLA-identical bone marrow transplantation has been successful.
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6/47. Oral leishmaniasis in a hiv-positive patient. Report of a case involving the palate.

    leishmaniasis is a parasitic disease caused by a protozoon (Leishmania), with different clinical forms that are endemic in certain countries. The association of this disease in patients who are seropositive to human immunodeficiency virus (hiv) has recently been described. leishmaniasis can develop in any stage of hiv infection, although the clinical manifestations - and hence the diagnosis - tend to coincide with the periods of maximum immune depression. We present the case of a hiv-positive, ex-intravenous drug abuser (in stage B2 of the CDC, 1992) with concomitant hepatitis c infection who presented with palatinal pain and bleeding for the past 2 months. Exploration revealed a vegetating tumoration of the hard palate. hematoxylin-eosin and Giemsa staining of the biopsy confirmed the diagnosis of leishmaniasis. The definitive diagnosis was mucocutaneous leishmaniasis (MCL), for a bone marrow aspirate proved negative, and no further lesions could be established. The patient was treated with meglumine antimoniate (Glucantime), followed by improvement of the lesions.
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7/47. Multiple insufficiency fractures with severe osteoporosis.

    Multiple insufficiency fracture is a rare injury. We report a 63-year-old woman who spontaneously developed insufficiency fractures at multiple sites including ribs, sacrum, pubis, ischium, acetabulum, metatarsal bone, and femoral neck. The patient had severe osteoporosis with a bone mineral density of 0.267 g/cm(2), although there was no evidence of bone metabolic disease or metastatic bone tumor. risk factors for osteoporosis in this case were her postmenopausal state and a history of gastrectomy. Interestingly, the serum level of insulin-like growth factor i, recognized as a growth factor that stimulates bone formation, was markedly decreased, and the patient had had viral hepatitis c. It was speculated that the synergistic effects of these disorders might have produced the osteoporosis, leading ultimately to the multiple insufficiency fractures.
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8/47. Pure red cell aplasia--report of 11 cases from eastern nepal.

    There were eleven cases of pure red cell aplasia diagnosed over a period of 2 years (January 2000-December 2001). All the patients had anemia with pallor and weakness being the presenting complaints. Hematological profile depicted normocytic normochromic anemia, reticulocytopenia and marked paucity of erythroid precursors on bone marrow aspiration and biopsy studies. In the present study, one case was of congenital pure red cell aplasia, in one other case of pyrexia of unknown origin, no definitive diagnosis could be made. Other associated diseases seen with pure red cell aplasia were thymoma, septicemia, protein energy malnutrition, non-Hodgkin's lymphoma, juvenile rheumatoid arthritis, acute myeloid leukemia, tuberculosis and hepatitis c. The association of pure red cell aplasia with haematologic malignancies is rare. There are very few case reports on pure red cell aplasia with hepatitis c.
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9/47. diagnosis of bronchiolitis obliterans organizing pneumonia after allogeneic bone marrow transplantation: case report.

    We report the case of a 40-year-old female patient after allogeneic bone marrow transplantation due to chronic myeloid leukaemia. One year after transplantation, the symptoms of recurrent bronchial and lung infections, inefficiently treated with antibiotics, appeared. The disease was further complicated due to hepatic insufficiency resulting from mixed infection with HBV and HCV as well as because of chronic graft-versus-host disease (GvHD). Chest computed tomography and pulmonary function tests seemed to confirm BOOP diagnosis, but despite three-time-conducted bronchoscopy, histopathological diagnosis was not obtained. When admitted to the Pulmonary Department, the patient was in serious condition caused by intensifying respiratory failure. After multidrug therapy enabling to control opportunistic infections, high doses of corticosteroids were administered intravenously resulting in partial health improvement. The patient seems to be afflicted with BOOP of mixed aetiology. Treatment efficiency may confirm the necessity of rapid BOOP diagnosis even if histopathological diagnosis is not obtainable.
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10/47. Case report: fulminant hepatitis c viral infection after allogeneic bone marrow transplantation.

    The authors describe two patients with acute leukemia who died of fulminant hepatitis caused by hepatitis c virus (HCV) after an allogeneic bone marrow transplant, the first such cases reported in japan. Both had developed posttransfusion hepatitis during chemotherapy to induce remission and for consolidation. Six months after blood transfusion, the blood serum of each patient was positive for HCV antibody and HCV rna. In each case, there was a transient improvement in liver function after the transplant. However, within 5 months of receiving the transplant and coincident with the withdrawal of cyclosporin A, each patient developed an acute exacerbation of hepatitis. The fulminant hepatitis in our patients may, therefore, have been caused by the reactivation of HCV induced by the immunosuppressive therapy followed by a reconstitution of the immune system.
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