33 research outputs found

    De Novo Superinfection of Hepatitis B Virus in an Anti-HBs Positive Patient with Recurrent Hepatitis C Following Liver Transplantation

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    A 60-year-old woman with end stage liver cirrhosis caused by genotype 2 hepatitis C virus (HCV) infection received an orthotopic liver transplantation (OLT). The patient was negative for the hepatitis B surface antigen (HBsAg) and positive for the anti-hepatitis B surface antibody (anti-HBs) prior to and one and a half months following the OLT. Due to reactivation of hepatitis C, treatment with interferon-alpha and Ribavirin started two months following the OLT and resulted in a sustained virological response. We performed a liver biopsy because a biochemical response was not achieved. Surprisingly, liver pathology showed HBsAg-positive hepatocytes with a lobular hepatitis feature, which had been negative in the liver biopsy specimen obtained one and a half months post-OLT. High titers of both HBsAg and HBeAg were detected, while anti-HBs antibodies were not found. Tests for IgM anti-hepatitis B core antibody and anti-delta virus antibodies were negative. The serum HBV DNA titer was over 1×107 copies/mL. A sequencing analysis showed no mutation in the "a" determinant region, but revealed a mixture of wild and mutant strains at an overlapping region of the S and P genes (S codon 213 (Leu/Ile); P codons 221 (Phe/Tyr) and 222 (Ala/Thr)). These findings suggest that de novo hepatitis B can develop in patients with HCV infection during the post-OLT period despite the presence of protective anti-HBs

    Comparison of seven prognostic tools to identify low-risk pulmonary embolism in patients aged <50 years

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    Does lamivudine prophylaxis eradicate persistent HBV DNA from allografts derived from anti-HBc-positive donors?

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    Transplantation of livers from anti-hepatitis B core anti-body (anti-HBc)-positive donors into anti-HBc-negative recipients is associated with a high rate of viral transmission. We report a prophylaxis regimen based on virologic evaluation of the donor. Liver and serum from hepatitis B surface antigen (HBsAg)-negative, anti-HBc-positive donors were evaluated by polymerase chain reaction (PCR) for hepatitis B virus (HBV) DNA. All anti-HBc-negative recipients were given a single dose of hepatitis B immunoglobulin (HBIG) during the anhepatic phase of transplantation and were placed on maintenance lamivudine monotherapy. Recipients were followed up longitudinally monitoring intrahepatic HBV DNA as well as serologic HBsAg and HBV DNA by PCR. Between January 1999 and August 2001, 14 anti-HBc-negative recipients received liver transplants from anti-HBc-positive donors. All donor serum was negative for HBV DNA. In total, nine of 14 (64%) livers had detectable HBV DNA; 1 patient was initially PCR-negative and low levels of HBV DNA were detected in a posttransplantation liver biopsy. Mean follow-up was 33 months (range, 22 to 51), and patient and graft survival were each 93%. One case of de novo hepatitis B occurred in a patient noncompliant with lamivudine, although all other serial serum HBsAg assay results were negative. Single-dose HBIG followed by maintenance lamivudine monotherapy prevented de novo hepatitis B in compliant patients. For the cohort of compliant patients that were initially HBV DNA-positive, 7 of 8 (88%) now have undetectable virus in the hepatic allograft by PCR analysis. Nevertheless, there is no evidence to suggest that viral eradication occurs. Accordingly, all patients are maintained on continued lamivudine prophylaxis

    Expanded Criteria Donors

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    The greatest challenge facing liver transplantation today is the shortage of donor livers. Demand far exceeds supply, and this deficit has driven expansion of what is considered an acceptable organ. The evolving standard has not come without costs, however, as each new frontier of expanded donor quality (i.e., advancing donor age, donation after cardiac death, and split liver) may have traded wait-list for post-transplant morbidity and mortality. This article delineates the nature and severity of risk associated with specific deceased donor liver characteristics and recommends strategies to maximally mitigate these risks
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