2% versus 48.5% in those randomized to 48 weeks). Thus, if an extended 72-week regimen is being contemplated for an individual patient, the decision should be informed by rs12979860 genotype status and should only be generally considered for slow responders who carry a T allele. Erlotinib research buy Interest in extended-duration therapy

is waning with the approval of the first direct-acting antiviral agents (DAAs). However, because slow virologic responders have suboptimal response rates to peginterferon/ribavirin/DAA triple therapy,28-31 response-guided therapy remains an important treatment strategy. A response-guided approach was used in the phase 3 studies of protease inhibitors by extending treatment to 48 weeks in patients with detectable HCV RNA at week 4 (telaprevir) or 8 (boceprevir).27,

28 These trials confirmed the potential for these agents to increase overall SVR rates and decrease treatment duration for many genotype 1 patients. A treatment extension beyond week 48 was not investigated so far. It is not clear, however, whether all patients will require a DAA to optimize treatment outcomes. For example, the addition of boceprevir after 4 weeks PARP inhibitor of treatment with peginterferon plus ribavirin improved SVR rates only in individuals with a <2-log10 drop in HCV RNA after the 4-week run-in period in a phase 2 study in treatment-naive genotype 1 patients.29 Furthermore, as shown in the present study, regardless of the IL28B genotype more than 80% of patients with an RVR on peginterferon/ribavirin achieve an SVR after just 24 weeks of treatment. Thus, the benefit of adding a DAA to standard peginterferon plus ribavirin therapy in these patients requires further evaluation. Like all published studies on the role of IL28B polymorphism, this analysis was carried out Ceramide glucosyltransferase retrospectively. Patients were

recruited for the parent trial between 2003 and 2008, long before the importance of the IL28B genotype in the treatment of chronic hepatitis C was established. Therefore, not all patients who were enrolled in the study were represented in the genotype analysis; thus, the results must be regarded with caution. Patients were recalled and asked to participate in this analysis; thereby only 62.3% of the study participants could be tested. This compares well with other retrospective trials (i.e., 65% in the study by Mangia et al.32 and 52.2% in the study by Thompson et al.17). The overall results of the parent study were not different from this subanalysis. Furthermore, patients were not stratified by rs12979860 genotype. It is reassuring that a similar proportion (≈60% to 67%) of patients were genotyped in each group, and that the relapse rates reported in groups A and B in the original study (33% and 17%, respectively) are generally similar to those reported in this analysis (38% and 19%, respectively).