Direct-acting antiviral agents in patients with hepatitis C genotype 1-4 infections in a tertiary hospital

Abstract

Objective: Hepatitis C virus (HCV) infection is a major cause of chronic liver disease. Six different genotypes (GT) of HCV (genotypes 1-6) have been identified. The genotype is clinically relevant since the majority of current direct antiviral agents (DAA´s) do not have pangenotypic efficacy. The purpose of this study was to describe the clinical characteristics of real world patients and evaluate the effectiveness of different treatment regimens.

Methods: Retrospective and observational study carried out in a third level hospital. Study period: January 2015-January 2016. Inclusion criteria: HCV patients of any genotype treated with either DAAs ± rivabirin (RBV) or DAAs + RBV + pegilated interferon (Peg-IFN) regimens for 12 weeks. Exclusion criteria: patients without adequate clinical or analytical information available for further analysis. Patients treated for 24 weeks were excluded. The main endpoint was sustained virologic response 12 weeks after the end of treatment (SVR12), and secondary endpoint was SVR24.

Results: A total of 515 patients were included (aged 55.52±8.97 years). GT1: patients treated with simeprevir + sofosbuvir (SIM + SOF), ledipavir (LDV)/SOF and paritaprevir/ritonavir/ombitasvir + dasabuvir (PTV/r/OBV + DSV) ± RBV had a SVR12 of 93.59% (190/203), 98.82% (N=84/85), 94.28% (66/70), respectively. Regarding daclatasvir (DCV) + SOF and SIM + DCV, everybody (19/19) and 87.5% (7/8) got SVR12, respectively. GT2: 71.42% (N=10/14) of patients achieved SVR12, concretely, SOF + RBV had a SVR12 75% (N=6/8). GT3: 43.75% (N=7/16), 90% (N=9/10) and 95% (N=19/20) of patients treated with LDV/SOF, LDV/SOF + RBV and SOF + DCV obtained SVR12, respectively. GT4: patients treated with LDV/SOF, SIM + SOF and PTV/r/OBV ± RBV had a SVR12 rate of 100% (21/21), 91.67% (22/24) and 92% (23/25), respectively. All patients that got SVR12 achieved SVR24.

Conclusions: Our study confirmed the efficacy data reported in clinical trials in a cohort of patients with GT1-4 and a wide range of basal characteristics.

Figure 1

SVR12 rates of HCV genotype 1-infected patients. SVR12 of all patients with chronic HCV genotype 1 infection treated with SIM+SOF (figure 1A), LDV/SOF (figure 1B), PTV/r/OBV+DSV±RBV (figure 1C), DCV+SOF (figure 1D) and SIM+DCV (figure 1E). SIM simeprevir, SOF sofosbuvir, LDV ledipasvir, PTV paritaprevir, r ritonavir, OBV ombitasvir, DSV dasabuvir, RBV ribavirin, DCV daclatasvir.

Figure 1

SVR12 rates of HCV genotype 1-infected patients. SVR12 of all patients with chronic HCV genotype 1 infection treated with SIM+SOF (figure 1A), LDV/SOF (figure 1B), PTV/r/OBV+DSV±RBV (figure 1C), DCV+SOF (figure 1D) and SIM+DCV (figure 1E). SIM simeprevir, SOF sofosbuvir, LDV ledipasvir, PTV paritaprevir, r ritonavir, OBV ombitasvir, DSV dasabuvir, RBV ribavirin, DCV daclatasvir.

Figure 2

SVR12 rates of HCV genotype 3-infected patients. It is represented the percentage of different subgroups of patients with HCV genotype 3 infection who achieved SVR12, treated with either LDV/SOF, or LDV/SOF + RBV, or DCV + SOF (LDV = ledipasvir, SOF = sofosbuvir, RBV = ribavirin, DCV =daclatasvir).

Figure 3

SVR12 rates of HCV genotype 4-infected patients It is represented the percentage of different subgroups of patients with HCV genotype 4 infection who achieved SVR12 treated with either SIM + SOF or LDV/SOF or PTV/r/OBV ± RBV (SIM = simeprevir, SOF = sofosbuvir, LDV = ledipasvir, PTV = paritaprevir, r = ritonavir, OBV = ombitasvir, RBV = ribavirin).\