Real-world effectiveness of daclatasvir plus sofosbuvir and velpatasvir/sofosbuvir in hepatitis C genotype 2 and 3

• Published in: Journal of hepatology 2019-01, Vol.70 (1), p.15-23
• Main Authors: Belperio, Pamela S., Shahoumian, Troy A., Loomis, Timothy P., Mole, Larry A., Backus, Lisa I.
• Format: Article
• Language: English
• Subjects: Antiviral Agents - therapeutic use; Carbamates - therapeutic use; Daclatasvir; DNA, Viral - genetics; Drug Therapy, Combination; Female; Follow-Up Studies; Genotype; Genotype & phenotype; Genotypes; Hepacivirus - genetics; Hepatitis; Hepatitis C; Hepatitis C, Chronic - drug therapy; Hepatitis C, Chronic - virology; Heterocyclic Compounds, 4 or More Rings - therapeutic use; Humans; Imidazoles - therapeutic use; Liver diseases; Male; Middle Aged; Patients; Registries; Retrospective Studies; Ribavirin; Sofosbuvir; Sofosbuvir - therapeutic use; Sustained virologic response; Treatment Outcome; Velpatasvir
• ISSN: 0168-8278; 1600-0641
• DOI: 10.1016/j.jhep.2018.09.018

[Display omitted] •In HCV genotype 2 or 3 patients, SVR rates with DCV + SOF were comparable to VEL/SOF.•SVR with DCV + SOF + RBV was comparable to SVR with VEL/SOF + RBV.•Regimen did not impact the odds of SVR for either HCV genotype 2 or genotype 3.•Results support using either DCV + SOF or VEL/SOF for HCV genotypes 2 and 3.•As guidelines have changed, some of the patients in this cohort were treated outside the current guidelines. Understanding the real-world effectiveness of all-oral hepatitis C virus (HCV) regimens informs treatment decisions. We evaluated the effectiveness of daclatasvir + sofosbuvir ± ribavirin (DCV + SOF ± RBV) and velpatasvir/sofosbuvir (VEL/SOF) ± RBV in patients with genotype 2 and genotype 3 infection treated in routine practice. This observational analysis was carried out in an intent-to-treat cohort of patients with HCV genotype 2 and genotype 3. Sustained virologic response (SVR) analysis was performed in 5,400 patients initiated on DCV + SOF ± RBV or VEL/SOF ± RBV at any Department of Veterans Affairs facility. For genotype 2, SVR rates did not differ between DCV + SOF (94.5%) and VEL/SOF (94.4%) or between DCV + SOF + RBV (88.1%) and VEL/SOF + RBV (89.5%). For genotype 3, SVR rates did not differ between DCV + SOF (90.8%) and VEL/SOF (92.0%) or between DCV + SOF + RBV (88.1%) and VEL/SOF + RBV (86.4%). In multivariate models of patients with genotype 2 and 3 infection, the treatment regimen was not a significant predictor of the odds of SVR. For genotype 3, significant predictors of reduced odds of SVR were prior HCV treatment-experience (odds ratio [OR] 0.51, 95% CI 0.36–0.72; p 3.25 (OR 0.60; 95%CI 0.43–0.84; p = 0.002) and a history of decompensated liver disease (OR 0.68; 95%CI 0.47–0.98; p = 0.04). For patients with genotype 2 and 3, treated with VEL/SOF ± RBV, 89% and 85% received 12-weeks of treatment, respectively. For DCV + SOF ± RBV, 56% and 20% of patients with HCV genotype 2 received 12-weeks and 24-weeks of treatment, respectively; while 53% and 23% of patients with HCV genotype 3 received 12-weeks and 24-weeks, with most direct-acting antiviral experienced patients receiving 24-weeks. In patients infected with HCV genotype 2 and 3, DCV + SOF ± RBV and VEL/SOF ± RBV produced similar SVR rates within each genotype, and the regimen did not have a significant impact on the odds of SVR. For patients with genotype 3, prior treatment-experience and advanced liver disease were significant predictors o