Background The current standard treatment for patients with chronic hepatitis C virus (HCV) infection is a combination of direct-acting antiviral agents(DAAs). Still, a relatively small amount of patients fail DAAs and there is not enough data to establish treatment recommendations for these cases.
Purpose The aim is to describe the efficacy of a second round of DAAs treatment for HCV infection after unsuccessful therapy with DAAs agents.
Material and methods An observational retrospective descriptive study was performed. The patients included in this study were diagnosed with HCV, underwent a first treatment with DAAs from September 2014 to March 2017, but did achieve sustained virological response 12 weeks after treatment (SVR12). The variables genotype, liver fibrosis (METAVIR score), first treatment with DAAs, SVR12 and second round of treatment, were extracted from electronic health records.
Results A total of 352 patients received treatment with DAAs and of these, 14 did not achieve SVR12. 4/14 did not receive new treatment, 3/14 received new treatment for 12 weeks and 7/14 for 24 weeks. The DAAs used were: simeprevir (SMV), sofosbuvir (SOF), ledipasvir (LED), ribavirina (RBV), dasabuvir (DSB), ombitasvir/paritaprevir/ritonavir (OMB/PTV/r), peginterferon (PEG), daclatasvir (DCV) and velpatasvir (VEL). The results by genotype were: genotype 1 (9/14): three patients had genotype 1a and six patients had genotype 1b. Regarding liver fibrosis diagnosis, five patients were F4, one patient was F3, two were patients F3 and one patient without Fibroscan®. Regarding treatment: 3/9 initially received SMV +SOF, and after SVR12 failure, 2/3 received LED/SOF +RBV and 1/3 received OMB/PTV/r+RBV. 2/9 received a first treatment with SMV +c +RBV and then LED/SOF +RBV. 1/9 received a first treatment with SOF +RBV and then DCV +SOF. 3/9 received initially LED/SOF and after failure, 1/3 received SMV +SOF + RBV, 1/3 received DCV +SMV +SOF and 1/3 did not receive new treatment.
Genotype 2 (1/14): one F4 patient received SOF+RBV and then DCV+SOF+ RBV.
Genotype 3 (3/14): two patients were F2 and 1 was F4. Patients first received DCV+SOF and then 2/3 received SOF/VEL+RBV, and 1/3 did not receive new treatment (currently under evaluation).
Genotype 4 (1/14): one F3 patient received LED/SOF and then SMV+SOF+ RBV.
Efficacy data were available for 10/14 patients and all of them achieved SVR12 with the second round of DAAs treatment.
Conclusion In patients who failed to achieve a SVR12 with first treatment, the second round of DAAs treatment was very successful. However, more data are necessary to establish strong recommendations.
No conflict of interest