The study of hepatitis C virus (HCV) kinetics after liver transplantation (LT) might be important to design strategies to prevent HCV infection of the graft. We analyzed HCV kinetics during and immediately after LT in 20 consecutive patients undergoing LT for HCV-related cirrhosis. HCV RNA was quantified in blood samples obtained at regular intervals before, during, and after transplantation. HCV-RNA concentrations decreased in 18 of 20 patients during the anhepatic phase (mean decay slope ؊0.92, mean HCV elimination half-life 2.2 hours). We found a significant correlation between the HCV viral load decay and the blood loss during the anhepatic phase, indicating that the observed HCV clearance rates are maximum estimates. In fact, in 1 patient with an unusually long anhepatic phase of 20 hours and with minimum blood loss, the HCV elimination half-life was 10.3 hours. Eight to 24 hours after graft reperfusion a sharp decrease in HCV viral load occurred in 19 patients (mean decay slope ؊0.34, mean HCV elimination half-life 3.44 hours). HCV RNA became undetectable in only 1 patient. During the following days, HCV-RNA concentrations increased rapidly in 10 patients (mean HCV doubling time 13.8 hours), remained at similar levels in 4, and continued to decrease in 6. The only variable associated with a second-phase viral load decay was the absence of corticosteroids as part of the immunosuppressive regimen. In conclusion, a sharp decrease in HCV viral load occurs during the anhepatic phase and immediately after graft reperfusion, most likely owing to a lack of virion production and hepatic viral clearance. HCV infection of the graft, however, is an extremely dynamic process and viral replication begins a few hours after LT. (HEPATOLOGY 2002;35: 680-687.) C irrhosis caused by hepatitis C virus (HCV) infection is the main indication of liver transplantation (LT) in most transplant programs. Infection of the liver graft after transplantation is almost universal and persistent infection leading to chronic hepatitis, cirrhosis, and graft failure is common. 1,2 In our geographic area, 30% of patients undergoing LT for HCV-related liver disease are already cirrhotic 5 years after transplantation. 3 Regretfully, prophylaxis of HCV infection of the graft is not feasible because no specific anti-HCV immune globulin is available. In addition, antiviral treatment in patients on waiting lists for LT appears to be poorly effective and may cause severe adverse effects. 4,5 Currently, treatment of hepatitis C infection after LT seems the most feasible strategy to eradicate HCV. 6-8 Treatment of HCV infection after LT can be initiated before liver damage occurs or once liver disease is already established. Treatment in the early phase of LT seems a reasonable approach because eradication of HCV would prevent liver damage. 9-11 However, there are only a few studies analyzing the efficacy of antiviral therapy in the early posttransplantation period. Interferon monotherapy is not effective in achieving sustained virologic response in ...

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The 2-year probability of presenting SR was significantly higher in LDLT compared to CLT (45% vs. 22%, P ‫؍‬ .019). By univariate analysis LDLT (P ‫؍‬ .019) and an ALT higher than 80 IU/L 3 months after LT (P ‫؍‬ .022) were predictors of SR. In 93 patients from whom a liver biopsy was available 3 months after LT, a lobular necroinflammatory score >1 (P < .01), LDLT (P < .01), and biliary complications (P ‫؍‬ .046) were associated with SR. However, the only variables independently associated with SR were LDLT (odds ratio [OR], ‫؍‬ 2.8; 95% CI,1.19-6.6; P ‫؍‬ .024) and a lobular necroinflammatory score >1 (OR, 3.1; 95% CI, 1.2-8; P ‫؍‬ .013). In conclusion, HCV recurrence is more severe in LDLT compared to CLT. Although our results were based on a single-center experience, they should be considered in the decision-making process of transplant programs, since severe HCV recurrence may ultimately compromise graft and patient survival. (HEPATOLOGY 2004; 40:699 -707.)

Cirrhosis, highly prevalent worldwide, develops after years of hepatic inflammation triggering progressive fibrosis. Currently, the main etiologies of cirrhosis are non-alcoholic fatty liver disease and alcohol-related liver disease, although chronic hepatitis B and C infections are still major etiological factors in some areas of the world. Recent studies have shown that liver fibrosis can

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The administration of angiotensin-blocking agents may be beneficial to reduce the development of graft fibrosis in hepatitis C recurrence after liver transplantation.

BackgroundHepatitis B virus (HBV) reactivation in patients with resolved HBV infection (HBsAg negative, antiHBc positive) is uncommon, but potentially fatal. The role of HBV prophylaxis in this setting is uncertain. The aim of this study was to compare the efficacy of tenofovir disoproxil fumarate (TDF) prophylaxis versus close monitoring in antiHBc-positive, HBsAg-negative patients under treatment with rituximab (RTX)-based regimens for hematologic malignancy.MethodsPREBLIN is a phase IV, randomized, prospective, open-label, multicenter, parallel-group trial conducted in 17 hospitals throughout Spain. Anti-HBc-positive, HBsAg-negative patients with undetectable HBV DNA were randomized to receive TDF 300 mg once daily (Group I) or observation (Group II). The primary endpoint was the percentage of patients showing HBV reactivation during 18 months following initiation of RTX treatment. Patients with detectable HBV DNA (Group III) received the same dose of TDF and were analyzed together with Group I to investigate TDF safety.ResultsSixty-one patients were enrolled in the study, 33 in the TDF treatment group and 28 in the observation group. By ITT analysis, HBV reactivation was 0% (0/33) in the study group and 10.7% (3/28) in the observation group (p = 0.091). None of the patients in either group showed significant differences in liver function parameters between baseline and the last follow-up sample. TDF was generally well tolerated and there were no severe treatment-related adverse events.ConclusionIn patients with hematological malignancy and resolved hepatitis B infection receiving RTX-based regimens, HBV reactivation did not occur in patients given TDF prophylaxis.