Impact of ribavirin priming on viral kinetics and treatment response in chronic hepatitis C genotype 1 infection. Issue 1 (21st June 2013)

• Record Type: Journal Article
• Authors: Mihm, U.; Welker, M.‐W.; Teuber, G.; Wedemeyer, H.; Berg, T.; Sarrazin, C.; Böhm, S.; Alshuth, U.; Herrmann, E.; Zeuzem, S.
• Is Part Of: Journal of viral hepatitis. Volume 21:Issue 1(2014)
• Page Start: 42
• Page End: 52
• Publication Date: 2013-06-21
• Subjects: Hepatitis, Viral -- Periodicals; Hepatitis, Viral, Animal; Hepatitis, Viral, Human; 616.3623
• DOI: 10.1111/jvh.12124
• Languages: English
• ISSNs: 1352-0504

Abstract

<abstract abstract-type="main" id="jvh12124-abs-0001"> <title>Summary</title> <p>Ribavirin amplifies the interferon‐alpha (IFN) signalling cascade. As ribavirin needs 4 weeks to reach steady state, ribavirin priming may optimize hepatic IFN sensitivity before starting a pegylated (PEG)‐IFN/ribavirin combination therapy. This study investigated potential benefits of ribavirin priming prior to PEG‐IFN2a/ribavirin combination therapy on viral kinetics, on‐treatment and sustained virological response (SVR) in chronic hepatitis C virus (HCV) genotype 1 infection. Sixty‐eight treatment naive patients were randomized 2:2:1 to ribavirin (ribavirin arm) or placebo (placebo arm) or PEG‐IFN2a (PEG‐IFN2a arm) for 6 weeks prior to 12 weeks of PEG‐IFN2a/ribavirin combination therapy within a double‐blind, placebo‐controlled trial. Then, standard PEG‐IFN2a/ribavirin combination therapy according to the German guidelines was continued under the responsibility of the investigators. Ribavirin was given according to body weight and PEG‐IFN2a at a dose of 180 μg subcutaneously once/week. During ribavirin priming, HCV RNA showed a decline of −0.58 log<sub>10</sub> IU/mL (<italic>P</italic> < 0.001) that was unrelated to the IL28B rs12979860 genotype (CC <italic>vs</italic> CT/TT, <italic>P</italic> = 0.244). Ribavirin priming did neither increase the PEG‐IFN2a‐induced first‐ or second‐phase viral decline (<italic>P</italic> values >0.100) nor on‐treatment response or SVR (HCV RNA undetectable at week 12 of combination therapy: ribavirin arm 56%, placebo arm 38%, PEG‐IFN2a arm 50%; SVR: ribavirin arm 41%, placebo arm 54%, PEG‐IFN2a arm 50%; <italic>P</italic> values >0.300). In conclusion, ribavirin monotherapy showed a significant antiviral activity that was not influenced by the IL28B genotype. Ribavirin priming prior to PEG‐IFN2a/ribavirin combination therapy did neither increase the first‐ or second‐phase viral decline nor on‐treatment response or SVR.</p> </abstract>