Abstract
Background:
Telaprevir (T, TVR) is a direct-acting antiviral (DAA) used for the treatment of genotype 1 chronic hepatitis C virus (HCV) infection. The sustained virological response (SVR) rates, i.e., undetectable HCV RNA levels 24 weeks after the end of treatment, is what differentiate treatments. This analysis evaluated the cost-effectiveness of TVR combined with pegylated interferon (Peg-IFN) alfa-2a plus ribavirin (RBV), with Peg-IFN and RBV (PR) alone or with boceprevir (B, BOC) plus Peg-IFN alfa-2b and RBV, in naïve patients.
Methods:
A Markov cohort model of chronic HCV disease progression reflected the pathway of naïve patients initiating anti-HCV therapy. SVR rates were derived from a mixed-treatment comparison including results from Phase II and III trials of TVR and BOC, and trials comparing both PR regimens. SVR has significant impact on survival, quality-of-life, and costs. Incremental cost per life year (LY) gained and quality-adjusted-life-year (QALY) gained were computed at lifetime, adopting the (National Health Service) NHS perspective. Cost and health outcomes were discounted at 3.5%. Uncertainty was assessed using deterministic and probabilistic sensitivity analyses. Sub-group analyses were also performed by interleukin (IL)-28B genotype and fibrosis stage.
Results:
Higher costs and improved outcomes were associated with T/PR relative to PR alone, resulting in an ICER of £12,733 per QALY gained. T/PR retained a significant SVR advantage over PR alone and was cost-effective regardless of IL-28B genotype and fibrosis stages. T/PR regimen ‘dominated’ B/PR, generating 0.2 additional QALYs and reducing lifetime cost by £2758. Sensitivity analyses consistently resulted in ICERs less than £30,000/QALY for the T/PR regimen over PR alone.
Limitations:
No head-to-head trial provides direct evidence of better efficacy of T/PR vs B/PR.
Conclusion:
The introduction of TVR-based therapy for genotype 1 HCV patients is cost-effective for naïve patients at the £30,000 willingness-to-pay threshold, regardless of IL-28B genotype or fibrosis stage.
Transparency
Declaration of funding
This analysis was funded by Janssen Pharmaceuticals. The authors confirm that the paper is an accurate representation of the study results. Several authors are employees of the sponsor and were involved in the study design, data collection and analysis, interpretation of data, writing of the report, and the decision to submit the paper for publication.
Declaration of interest
SC and FB are employees of OptumInsight, who received funding from Janssen Pharmaceuticals. SG, SC, and SL are employees of Janssen Pharmaceuticals. GD has received consulting fees from Roche, Merck, and Janssen pharmaceuticals
Acknowledgments
We thank Joanne Williams and Catherine Elliott (Gardiner-Caldwell Communications) for general editing/styling and co-ordination support (funded by Janssen Pharmaceuticals).
Author contributions
CS, FB, SG, and GD were involved in designing these analyses; SC and SL were involved in the collection, analysis, and interpretation of data; SC and SL wrote the first draft of the report, which was subsequently critically reviewed by all authors; all authors were involved in the decision to submit the paper for publication.