Başkent Üniversitesi Yayınları

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    Recurrence of Hepatitis C Virus (Genotype 4) Infection After Living-Donor Liver Transplant in Egyptian Patients
    (Başkent Üniversitesi, 2009-09) Kamel, Sanaa; El-Gabaly, Hatem; Yosry, Ayman; Abdel-Rahman, Mahasen; Esmat, Gamal; El-Serafy, Magdy; Omar, Ashraf; Doss, Waheed; Zayed, Nagla; Said, Mohamed; Ismail, Tamer; Hosny, Adel; Marawan, Ebrahem; El-Malt, Osama; Kamel, Refaat Refaat; Hatata, Yaser; El-Taweel, Ahmad; Ghali, Ahmad; Sabri, Hussein
    Objectives: The recurrence of hepatitis C virus infection after liver transplant is common and may endanger both graft and patient survival. We investigated the frequency and outcome of and risk factors for the recurrence of that virus after living-donor liver transplant in hepatitis C virus positive recipients. Materials and Methods: Seventy-four adult hepatitis C virus positive subjects were monitored for 36 months after living-donor liver transplant and demographic and laboratory data for the recipients and donors were evaluated. Recurrent hepatitis C virus infection was diagnosed on the basis of viral replication revealed by polymerase chain reaction after transplant, elevated levels of transaminases, and the results of liver biopsy. Results: Hepatitis C virus recurrence was identified in 31.1% of the patients studied. Histopathologic recurrence was mild, and 91% of the subjects had a fibrosis score of ≤ F2. No recipient exhibited cirrhosis or clinical decompensation during follow-up. Recurrent hepatitis C virus infection was associated with pretransplant and posttransplant viral load and antibody positive to hepatitis B core antigen. No other risk factors (sex, donor or recipient age, pretransplant Child-Pugh or Model for End-Stage Liver Disease scores, immunosuppressive drug therapy, and treatment with pulse steroids) were significantly correlated with the frequency of hepatitis C virus recurrence, the grade of the histologic activity index, or the stage of fibrosis. Conclusions: In living-donor liver transplant recipients, patient and graft survival rates associated with hepatitis C virus (genotype 4) related cirrhosis were comparable to those in deceased-donor liver transplant recipients reported in the literature. Recurrent infection with hepatitic C virus after living-donor liver transplant was mild. After transplant, a higher viral load and the presence of antibody to hepatitis B core antigen could be risk factors for hepatitis C virus recurrence. Long-term follow-up in a large number of patients is required.
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    HCV Antibody Quantitative Levels in Liver Transplant Patients: Do They Have Any Relevance in Clinical Practice?
    (Başkent Üniversitesi, 2006-06) Jain, Ashok; Menegus, Marilyn; Mohanka, Ravi; Orloff, Mark; Abt, Peter; Mantry, Parvez; Bozorgzadeh, Adel
    Objectives: Hepatitis C virus (HCV) is not directly cytopathic to the hepatocytes; however, host immune response against the virus does cause hepatic injury. Production of the HCV antibody is a host immune response to a viral antigen. The currently used HCV antibody assay is a qualitative, not quantitative, assessment. In this study, we sought to quantitatively estimate HCV antibody levels in patients who had undergone liver transplantations at the University of Rochester Medical Center, Rochester, New York, and correlate these levels with HCV RNA viral load, genotype, severity of recurrence, and anti-HCV treatment. Materials and Methods: From 39 liver transplantation patients, we obtained 141 blood samples for quantitative HCV RNA to measure HCV antibody levels quantitatively. Results: Most antibody levels were within a narrow range with a mean of 32.9 ± 5.1. Samples with undetectable RNA had a mean antibody level of 31.4 ± 8.0, and samples with a positive RNA had mean level of 33.0 ± 4.6. The mean antibody levels were significantly higher for patients with genotype 1 (n = 33) compared with those with genotype 2 (n = 5) (33.2 vs 29.1; P = .007). No correlation was found between antibody levels and severity of hepatic injury with regard to hepatitis activity index or fibrosis score. Six patients with no response to anti-HCV treatment had no change in their mean antibody levels (33.7 vs 34.5). Ten patients who responded to anti-HCV therapy had lower mean levels after therapy, but the changes were not significant (34.2 vs 30.4). Conclusions: Antibody levels in this study did not correlate with viral load or hepatic injury. However, genotype-2 patients had significantly lower levels compared with genotype-1 patients, and patients who responded to anti-HCV therapy demonstrated decreased antibody levels.