15-17 Individuals with a C/C genotype were more likely to achieve an RVR and an SVR than patients who carry the T allele. However, not all patients with a C/C genotype achieve an RVR and an SVR, and not all patients with
a T allele are slow responders. Overall, approximately 50% of patients with a C/C genotype achieved an RVR and, regardless of the on-treatment response, approximately 83% of those with an EoT response achieved an SVR. Among patients with a T allele, approximately 16% achieved an RVR and the overall SVR rate in those with an EoT response was 72%. Although a much higher proportion of patients with a C/C genotype achieved an RVR compared with carriers of a T allele, SVR rates were similar
DAPT nmr Carfilzomib in vivo in patients with an RVR regardless of genotype. Interestingly, among patients with an RVR the majority of those with a C/C genotype (64%) had a baseline HCV RNA level ≥400,000 IU/mL and the majority of those with a T allele (79%) had a baseline HCV RNA level <400,000 IU/mL. This is consistent with previous reports that patients with C/C genotype have higher mean viral loads than patients who carry a T allele.13, 17 These findings confirm that achievement of an RVR at week 4 is the best predictor of SVR in patients receiving pegylated interferon plus ribavirin therapy.24 Although IL28B genotype is the best pretreatment predictor of SVR, the addition of this variable results in, at best, marginal improvement in the positive predictive value of RVR for SVR.24 The IL28B polymorphism explains only part of the response to interferon-based therapies. It has recently been suggested that increased expression of interferon-stimulated genes is a better predictor of nonresponse than IL28B polymorphism alone.25,
26 Thus, there may be scope to further improve the ability to predict response before treatment is initiated. The results suggest that extension of treatment to 72 weeks in HCV genotype 1 and 4 patients with a slow response may decrease relapse rates in patients Methamphetamine who carry a T allele, whereas patients with a C/C genotype derived little benefit from treatment extension. Relapse rate was the primary endpoint of the parent study. Calculation of SVR rates by ITT analysis is difficult because patients not completing the assigned treatment had to be considered treatment failures. As in the parent study, by ITT analysis, lower relapse rates did not result in significantly higher SVR rates. Indeed, when the data were subjected to an ITT analysis the SVR rates were actually lower in patients with a C/C genotype who achieved an EVR but no RVR and were randomized to extended treatment (52.2% versus 70.4% in those randomized to 48 weeks). This suggests that the higher withdrawal rate with extended therapy (with patients being imputed as SVR failures) is not offset by an increased SVR rate in C/C patients.