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1/144. Liver damage induced by coumarin anticoagulants.

    Except for bleeding complications, relevant adverse effects of coumarin anticoagulants are comparatively rare considering the widespread use of these substances. Here we present the case of a 56-year-old woman who developed recurrent episodes of severe hepatitis following repeated exposure to phenprocoumon (Marcumar; Roche, Grenzach-Wyhlen, germany) and warfarin (Coumadin; DuPont Pharma, Bad Homburg, germany) after replacement of the mitral valve with a mechanical prosthesis. The diagnosis of "coumarin-induced hepatitis" is compatible with the time relationship between start of the drug and the onset of hepatopathy (first episode 8 months, second episode 4 weeks, and third episode 7 days), the rapid improvement following discontinuation of the drug, recurrence of liver dysfunction after re-exposure to the drug, and liver histology. After anticoagulant therapy was changed to heparin and acenocoumarol (Sintrom; Ciba-Geigy, Basel, switzerland), the patient's general state was markedly improved and her liver values became almost normal. This case will be discussed and compared with other reports of coumarin-induced hepatic lesions. Although liver damage induced by coumarin derivates is rare, it is important to be aware of the hepatotoxic potential of these drugs, which, in most cases, mimics the clinical presentation of viral hepatitis.
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ranking = 1
keywords = hepatitis
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2/144. Three cases of severe subfulminant hepatitis in heart-transplanted patients after nosocomial transmission of a mutant hepatitis b virus.

    Fulminant and severe viral hepatitis are frequently associated with mutant hepatitis b virus (HBV) strains. In this study, the genetic background of a viral strain causing severe subfulminant outcome in heart-transplanted patients was studied and compared with viral hepatitis B strains that were not linked to severe liver disease in the same setting. A total of 46 patients infected nosocomially with HBV genotype A were studied. Five different viral strains were detected, infecting 3, 9, 5, 24, and 5 patients, respectively. Only one viral strain was found to be associated with the subfulminant outcome and 3 patient deaths as a consequence of severe liver disease. The remaining 43 patients with posttransplantation HBV infection did not show this fatal outcome. Instead, symptoms of hepatitis were generally mild or clinically undiagnosed. Comparison of this virus genome with the four other strains showed an accumulation of mutations in the basic core promoter, a region that influences viral replication, but also in hepatitis B X protein (HBX) (7 mutant motifs), core (10 mutant motifs), the preS1 region (5 mutant motifs), and the HBpolymerase open reading frame (17 motifs). Some of these variations, such as those in the core region, were located on the tip of the protruding spike of the viral capsid (codons 60 to 90), also known in part as an important HLA class II-restricted epitope region. These mutations might therefore influence the immune-mediated response. The viral strain causing subfulminant hepatitis was, in addition, the only strain with a preCore stop codon mutation and, thus, hepatitis B e antigen (HBeAg) expression was never observed. The combination of these specific viral factors is thought to be responsible for the fatal outcome in these immune-suppressed heart-transplant recipients.
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ranking = 5
keywords = hepatitis
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3/144. Development of autoimmune hepatitis following liver transplantation for primary biliary cirrhosis.

    Two patients undergoing liver transplantation for classical end-stage primary biliary cirrhosis (PBC) are described, who went on to develop de novo autoimmune hepatitis (AIH) in the transplanted liver. The presentation, in both instances, was with malaise and lethargy. Markedly elevated serum transaminases were found, together with a raised serum IgG and/or globulin fraction and histological features on liver biopsy typical of AIH. Both cases had had changes in their immunosuppressive therapy before the onset of AIH episodes, and both rapidly responded to reinstitution of steroid therapy. The finding, in each case, of a coincidental multiple HLA class I allele match between the recipient and their liver donor suggests that HLA class I-restricted mechanisms may play an important role in the pathogenesis of AIH.
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ranking = 1.6666666666667
keywords = hepatitis
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4/144. Successful recanalization of late portal vein thrombosis after liver transplantation using systemic low-dose recombinant tissue plasminogen activator.

    portal vein thrombosis (PVT) is an infrequent complication following hepatic transplantation. However, deterioration of liver function and accompanying complications may be life threatening. Several attempts of surgical or percutaneous transhepatic procedures have been described. In some cases high dose fibrinolytic regimens have been successful. We describe the case of a male liver recipient with recurrent liver fibrosis due to hepatitis B reinfection and late portal vein thrombosis 45 months after transplantation. Complete recanalization was achieved using systemic low dose recombinant tissue plasminogen activator (rt-PA).
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ranking = 0.33333333333333
keywords = hepatitis
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5/144. Transmission of hepatitis c virus from a surgeon to a patient. The Incident Control Team.

    An investigation was carried out to find the source of infection in a patient who developed hepatitis c virus (HCV) infection after cardiothoracic surgery, and to determine whether other patients had become infected. Virological tests on specimens from the patient and potential sources (blood donors and members of the surgical team) showed that the patient and the surgeon who acted as first assistant were infected with HCV of the same genotype: 4a. No other source of infection was identified. Ninety-one per cent (277) of the 304 other exposed patients available for follow up were tested--none had antibody to HCV. It was concluded that hepatitis c may be transmitted from surgeon to patient during exposure prone procedures, and that the transmission rate in this incident was 0.36% (1/278; 95% confidence interval 0.0061%-1.98%).
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ranking = 2
keywords = hepatitis
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6/144. Outcome of lamivudine resistant hepatitis b virus infection in the liver transplant recipient.

    BACKGROUND: In many transplant centres lamivudine is an important component of prophylaxis against, and treatment of, hepatitis b virus (HBV) graft infection. Drug resistant HBV species with specific polymerase mutations may emerge during lamivudine treatment. AIMS: To examine the clinical consequences of graft infection by lamivudine resistant virus. methods: The clinical course of four liver transplant patients who developed graft infection with lamivudine resistant virus was reviewed. The response of HBV infection to reduction of immunosuppression and to manipulation of antiviral therapy was assessed. For each patient, serum viral titre was measured and the viral polymerase gene was sequenced at multiple time points. RESULTS: High serum titres were observed following emergence of the lamivudine resistant species. Wild type HBV re-emerged as the dominant serum species after lamivudine withdrawal. All patients developed liver failure, and onset of liver dysfunction was observed when resistant virus was the dominant serum species. In three patients, liver recovery was observed when immunosuppression was stopped and when alternative antivirals were given. Wild type virus appeared to respond to ganciclovir, and to reintroduction of lamivudine. For one patient, introduction of famciclovir was associated with clinical, virological, and histological response. CONCLUSIONS: Failure of lamivudine prophylaxis may identify patients at special risk for the development of severe graft infection. Treatment of graft reinfection should include reduction of immunosuppression, and systematic exposure to alternative antivirals. Viral quantitation and genetic sequencing are essential components of therapeutic monitoring.
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ranking = 1.6666666666667
keywords = hepatitis
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7/144. recurrence of hepatitis B after single lung transplantation.

    This study describes a patient who developed decompensated liver disease secondary to reactivation of hepatitis B infection 20 months after single lung transplantation following augmentation of immunosuppression to treat allograft rejection. Discussion focuses on the virologic and management issues of this case and reviews the approach taken when considering patients with chronic hepatitis B infection for lung transplantation.
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ranking = 2
keywords = hepatitis
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8/144. liver failure with steatonecrosis after jejunoileal bypass: recovery with parenteral nutriton and reanastomosis.

    Two women, aged 41 and 51 years, developed jaundice, encephalopathy, and hypoprothrombinemia during rapid weight loss four and 12 months after jejunoileal bypass for refractory obesity. Both were treated for liver failure and received a prolonged course of nutrition parenterally and orally. Serial liver biopsy specimens demonstrated extensive alcoholic-like hepatitis and cirrhosis that improved with nutritional repletion and reanastomosis. Postoperative biopsy specimens later demonstrated minimal portal fibrosis in one patient and inactive mild cirrhosis in the other. Although previous reports indicate that patients usually die when they develop liver failure of this severity after jejunoileal bypass, prolonged intensive nutritional repletion was associated with sufficient clinical and histologic improvement in these two patients so that intestinal reanastomosis could be performed safely.
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ranking = 0.33333333333333
keywords = hepatitis
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9/144. Recurrent type I membranoproliferative glomerulonephritis in a renal allograft: successful treatment with plasmapheresis.

    Recurrent disease is increasingly recognized as a cause of renal allograft dysfunction and failure. We describe a patient with type I membranoproliferative glomerulonephritis not associated with hepatitis c. The glomerular disease recurred in the renal allograft within 1 month of transplantation, leading to acute allograft dysfunction and nephrotic syndrome. Aggressive treatment with prednisone and plasmapheresis resulted in improvement in kidney function, improvement of the light microscopic picture, and removal of immune complexes from the glomerular subendothelial space.
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ranking = 0.33333333333333
keywords = hepatitis
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10/144. lamivudine for treating active hepatitis B in renal transplant recipients: a case report.

    AIM: Chronic hepatitis B is still a matter of concern among renal transplantation patients and patients waiting for a renal transplant since it influences negatively morbidity and mortality. morbidity and mortality are associated with HBV replication. lamivudine is a new antiviral agent whose use has been advocated to treat HBV-infected liver transplanted patients. SUBJECT AND methods: Here we present our experience with an HBV-positive kidney-liver transplanted patient treated with lamivudine after transplantation. RESULTS: After lamivudine was started HBV-dna became negative (chemiluminescence, Digene Hybrid Capture System, USA 1997) and ALT levels returned to normal. After eighteen months and after steroid pulses treatment for acute rejection, HBV-dna became positive again, probably due to virus mutation. lamivudine treatment was not withdrawn since it has been suggested that the mutant form might be less pathogenic than the wild one. To this extent, more than 10 months after, our patient is still in a good clinical general condition and still takes lamivudine 75 mg/day. No lamivudine-related side effects were recorded. CONCLUSIONS: Our case confirms that lamivudine is a safe and useful tool in treating renal transplant recipients with chronic hepatitis B.
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ranking = 2
keywords = hepatitis
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