This article was accepted for publication after full peer-review.
Telaprevir or boceprevir triple therapy in patients with chronic hepatitis C and varying severity of cirrhosis
Article first published online: 23 MAR 2014
© 2014 John Wiley & Sons Ltd
Alimentary Pharmacology & Therapeutics
Volume 39, Issue 10, pages 1213–1224, May 2014
How to Cite
Saxena, V., Manos, M. M., Yee, H. S., Catalli, L., Wayne, E., Murphy, R. C., Shvachko, V. A., Pauly, M. P., Chua, J., Monto, A. and Terrault, N. A. (2014), Telaprevir or boceprevir triple therapy in patients with chronic hepatitis C and varying severity of cirrhosis. Alimentary Pharmacology & Therapeutics, 39: 1213–1224. doi: 10.1111/apt.12718
- Issue published online: 16 APR 2014
- Article first published online: 23 MAR 2014
- Manuscript Accepted: 1 MAR 2014
- Manuscript Revised: 25 FEB 2014
- Manuscript Revised: 16 FEB 2014
- Manuscript Received: 24 JAN 2014
- NIH. Grant Number: T32 DK060414
- VA Merit Funding. Grant Number: 1I01 CX000295-01A1
- Liver Center. Grant Number: NIH P30 DK 026743
Risks and benefits of protease inhibitor (PI) (telaprevir or boceprevir) triple therapy in hepatitis C virus (HCV)-infected patients with mildly decompensated cirrhosis, including those wait-listed for liver transplantation (LT), are incompletely known.
To assess virological responses and safety of PI triple therapy in patients with mildly decompensated Child-Pugh (CP) CP ≥6 vs. compensated (CP = 5) cirrhosis.
Multicentre cohort of 160 adults with cirrhosis treated with peginterferon/ribavirin (peg-IFN/RBV) plus telaprevir (69%) or boceprevir (31%), comparing outcomes between those with CP = 5 and CP ≥6.
Patients, 47% with CP ≥6 cirrhosis (CP range 6–10), received PI triple therapy for a targeted duration of 48 weeks. The cohort was median age 59 years, 32% female, 59% genotype 1a, 35% previous null/partial responders. Sustained virological response at 12 weeks (SVR12) was achieved by 35% of patients with CP ≥6 vs. 54% of those with CP = 5 (P = 0.02). CP = 5, achievement of rapid virological response and genotype 1b/other, independently predicted SVR12. Compared to those with CP = 5, patients with CP ≥6 had more peg-IFN dose reductions, eltrombopag use, transfusions and hospitalisations to manage adverse events (all P < 0.05). Overall, 67 (42%) discontinued treatment early. Nine wait-listed patients were treated for a median of 97 days (IQR 60–160) prior to liver transplantation and five achieved post-LT SVR.
In the presence of mild decompensation (Child-Pugh ≥6), SVR12 rates with protease inhibitor triple therapy are significantly reduced and adverse events increased. Thus, treatment with protease inhibitor triple therapy, if judged as necessary, should be undertaken with close monitoring and awareness of the significant risks.