Combined Antiviral Therapy for Recurrent Hepatitis C Virus After Liver Transplantation

Abstract

tients in the Grossberg study) is unjustifiable.Furthermore, the results by quintile presented in Table 1, abstracted from text in the Grossberg paper and corrected by the corresponding author, indicate that the proportion of patients with predicted probability less than 0.20 is 0.065 (95% confidence interval: 0.028 -0.102). This is in sharp contrast to the proportion of patients with predicted probability less than 0.20 calculated from Irish and colleagues, 0.453. Because the predicted probability is conditional on observed covariates measured at time of transplantation (e.g., donor age and cold ischemia time), any difference in predicted probability is related to differences in study sample characteristics. Thus, the sample used by Grossberg cannot be used to validate or disprove the Irish DGF nomogram.The authors conclusion that the Irish nomogram is "weakly predictive" is based on misinterpretation of the numeric degree of difference between mean values.The mean difference between the DGF group and the No-DGF group is reported as 0.04. If we multiply the DGF risk score by 1,000, for example, then the mean difference between the two groups is 40. Although the magnitude of the difference has increased 1,000-fold, the sensitivity and specificity of the model, or its ability to discriminate, have not changed.Thus, we believe that, based on inappropriate use of validation methods and disparate study sample characteristics, the Grossberg study does not invalidate the Irish DGF nomogram. The Irish DGF nomogram remains useful for prediction of the likelihood of DGF but not its absolute occurrence.

Survival study and treatment strategy for second primary tumors in the oral cavity in patients with nasopharyngeal carcinoma after definitive radiation

“…To further study the impact of HCV infection after liver transplantation, we analyzed the levels of CD4 + CD25 + CD45RO + IL‐7Rα high T cells before and after antiviral therapy both in responders (ie, those who became HCV RNA–negative) and in nonresponders (ie, those who were persistently HCV RNA–positive despite antiviral therapy). All recipients were treated according to a previously described protocol with pegylated interferon and ribavirin 16. In responders, we observed a significant increase in CD4 + CD25 + CD45RO + IL‐7Rα high T cells in comparison with nonresponders, in whom levels of CD4 + CD25 + CD45RO + IL‐7Rα high T cells remained unmodified.…”

“…All HCV‐infected transplant recipients (n = 29) had a persistent HCV infection (viremia) after liver transplantation. During the study, 10 HCV‐infected liver transplant recipients, who had characteristic biochemical HCV hepatitis with biopsy‐proven allograft HCV recurrence, were treated with lower dose combined antiviral therapy consisting of pegylated interferon alpha 2a (Pegasys, Hoffmann‐La Roche, Switzerland; 135 μg/week) and ribavirin (Copegus, Hoffmann‐La Roche; 200‐400 mg/day), as previously described 16. The antiviral therapy was planned for 12 months; this depended on the genotype (ie, 6 months for patients with genotypes 2 and 3) and tolerability.…”

Antiviral Treatment of Patients with Recurrent Hepatitis C After Liver Transplantation with Pegylated Interferon

“…Pegylated IFNa in combination with RBV significantly improved the antiviral response rates in the treatment of naive patients with chronic HCV infection [12] and have been shown to be safe and effective in liver transplant recipients, reaching sustained virological response (SVR) rates of up to 40% for all genotypes [13][14][15][16][17][18][19][20][21][22]. Antiviral therapies can be conducted pre-OLT, preemptively in the early posttransplant period, and when HCV recurrence has developed.…”