Randomised clinical trial: the efficacy of treatment, guided by a shorter duration of response, using peginterferon alfa-2a plus ribavirin for hepatitis C virus other than genotypes 2 or 3
Article first published online: 2 NOV 2011
© 2011 Blackwell Publishing Ltd
Alimentary Pharmacology & Therapeutics
Volume 35, Issue 1, pages 37–47, January 2012
How to Cite
Lee, S. S., Sherman, M., Ramji, A., Greenbloom, S., Elkashab, M., Pluta, H., Hilzenrat, N., Balshaw, R., Usaty, C. and Myers, R. P. (2012), Randomised clinical trial: the efficacy of treatment, guided by a shorter duration of response, using peginterferon alfa-2a plus ribavirin for hepatitis C virus other than genotypes 2 or 3. Alimentary Pharmacology & Therapeutics, 35: 37–47. doi: 10.1111/j.1365-2036.2011.04911.x
- Issue published online: 9 DEC 2011
- Article first published online: 2 NOV 2011
- Publication data Submitted 14 July 2011 First decision 14 August 2011 Resubmitted 10 October 2011 Accepted 11 October 2011 EV Pub Online 2 November 2011
Aliment Pharmacol Ther 2012; 35: 37–47
Background The efficacy of individualised antiviral treatment durations for chronic hepatitis C remains unclear.
Aim To evaluate treatment durations based on virological responses at week 4, 8 and 12 of peginterferon alfa-2a plus ribavirin therapy.
Methods Previously untreated patients with HCV genotypes, other than 2 or 3, initiated therapy with peginterferon alfa-2a 180 μg/week plus ribavirin 1000–1400 mg/day. HCV-RNA-negative patients at week 4 rapid virological response (RVR) were randomised to 24 or 48 weeks of treatment; those negative at week 8 were randomised to 36 or 48 weeks; and those who were negative or had a ≥2-log drop at week 12 were randomised to 72 or 48 weeks. Sustained virological response (SVR) was defined as undetectable HCV-RNA after 24 weeks of follow-up.
Results The study was terminated prematurely due to lagging enrolment. Of 236 patients who started treatment, 195 were randomised at week 4 (n = 50), 8 (n = 61) or 12 (n = 84). Ninety-five per cent of patients had genotype 1. SVR rates were not significantly different between patients randomised to 24 (84%) or 48 weeks (84%) at week 4, to 36 (73%) or 48 weeks (74%) at week 8, or to 48 (49%) or 72 weeks (40%) at week 12.
Conclusions In this predominantly genotype 1 cohort, shortening therapy to 24 weeks in patients with a week-4 response and 36 weeks in those with a week-8 response produced SVR rates that were similar to a 48-week regimen. Lengthening treatment to 72 weeks did not improve SVR rates. Genotype 1 patients with RVR can be treated for 24 weeks (clinicaltrials.gov NCT00483938).