38 research outputs found

    New all‐oral HCV therapies for genotype 1: A final good‐bye to interferon

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/107533/1/cld369.pd

    Interview with american association for the study of liver diseases president Dr. Anna Lok

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    Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/136704/1/hep41038.pd

    NAM 2017 report: A national plan to eliminate hepatitis B and C in the United States by 2030 and the AASLD’s response

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    Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/138352/1/hep29361.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/138352/2/hep29361_am.pd

    Antiviral therapy in chronic hepatitis B viral infection during pregnancy: A systematic review and meta‐analysis

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    Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/137739/1/hep28302.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/137739/2/hep28302-sup-0001-suppinfo01.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/137739/3/hep28302_am.pd

    Combination of HBIG and lamivudine-resistant mutations: A formula for trouble?

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    Background & Aims: Lamivudine has become a main therapeutic option for treating hepatitis B virus (HBV) infection. Although drug resistance develops, the clinical course after selection of antiviral-resistant HBV mutants seems to be benign. However, we observed a severe clinical course of hepatitis B infection in several liver transplant recipients after the emergence of lamivudine resistance. This was associated with high viral load in the blood. Methods: In this report, we characterize the molecular mechanisms underlying drug-dependent enhanced replication of particular lamivudine-resistant HBV mutants selected in these patients, which were associated with sudden onset of liver failure. Results: The clinical course was characterized by a sudden rise in serum bilirubin, prothrombin time, and transaminase. HBV sequence analysis of these patients revealed both mutations in the “a-determinant” of the envelope and the YMDD (tyrosine, methionine, aspartate, aspartate) motif (domain C) of the polymerase protein. Transfection experiments with replication competent vectors indicated that the “a-determinant” changes were not associated with resistance, whereas mutations in the YMDD motif conferred resistance to lamivudine. More importantly, combinations of mutations in the “a-determinant” and the YMDD motif in patients with a severe hepatitis were not only resistant to lamivudine treatment, but showed enhanced replication in vitro in the presence of lamivudine. This observation was confirmed in separate laboratories. Conclusions: Severe and fatal hepatitis B infection can occur during lamivudine therapy and may be associated with certain HBV mutants selected during sequential nucleoside and HBIg treatment. The lamivudine-enhanced replication shown by these mutants suggests that continuation of therapy with lamivudine could be deleterious in some patients.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/35279/1/500081118_ftp.pd

    Outcomes in hepatitis C virus–infected recipients of living donor vs. deceased donor liver transplantation

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    In this retrospective study of hepatitis C virus (HCV)–infected transplant recipients in the 9-center Adult to Adult Living Donor Liver Transplantation Cohort Study, graft and patient survival and the development of advanced fibrosis were compared among 181 living donor liver transplant (LDLT) recipients and 94 deceased donor liver transplant (DDLT) recipients. Overall 3-year graft and patient survival were 68% and 74% in LDLT, and 80% and 82% in DDLT, respectively. Graft survival, but not patient survival, was significantly lower for LDLT compared to DDLT ( P = 0.04 and P = 0.20, respectively). Further analyses demonstrated lower graft and patient survival among the first 20 LDLT cases at each center (LDLT 20; P = 0.002 and P = 0.002, respectively) and DDLT recipients ( P 20 and DDLT were not significantly different ( P = 0.66 and P = 0.74, respectively). Overall, 3-year graft survival for DDLT, LDLT >20, and LDLT 20 were not significantly different. Important predictors of graft loss in HCV-infected patients were limited LDLT experience, pretransplant HCC, and higher MELD at transplantation. Liver Transpl 13:122–129, 2007. © 2006 AASLD.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/55915/1/20995_ftp.pd

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    Improvement of predictive models of risk of disease progression in chronic hepatitis C by incorporating longitudinal data

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    Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/111798/1/hep27750.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/111798/2/hep27750-sup-0001-suppinfo01.pd
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