Prediction of a sustained viral response in chronic hepatitis C patients who undergo induction therapy with double filtration plasmapheresis plus interferon-β/ribavirin

Exp Ther Med. 2015 May;9(5):1646-1650. doi: 10.3892/etm.2015.2340. Epub 2015 Mar 10.

Abstract

The aim of the present study was to determine predictors of a sustained virological response (SVR) with a regimen of double filtration plasmapheresis (DFPP) combined with interferon-β plus ribavirin (IFN-β/RBV) induction therapy prior to pegylated (PEG-IFN/RBV) standard of care (SOC) therapy for patients with chronic hepatitis C who had experienced SOC treatment failure. Predictors of a SVR were analyzed in chronic hepatitis C patients with genotype 1b hepatitis C virus (HCV), who had a high viral load. The patients had been unresponsive to previous IFN therapy and underwent induction therapy with IFN-β/RBV plus DFPP, which was performed five times during the same period, followed by PEG-IFN/RBV. In total, 10 patients received the combination DFPP plus IFN-β/RBV induction therapy prior to PEG-IFN/RBV therapy for the treatment of chronic hepatitis C. Two weeks after treatment initiation, a decrease in the HCV RNA levels of ≥2 log IU/ml occurred in 9/10 patients (90%), while a decrease of ≥4 log IU/ml was observed in 4/10 patients (40%). The HCV RNA levels at week 2 after treatment initiation in the SVR and non-SVR patients decreased by 5.0±0.8 and 2.9±1.1 log IU/ml, respectively. Despite no response to previous IFN therapy, three of the 10 patients (30%) experienced a SVR. The results indicated that a rapid virological response ensued following IFN-β/RBV induction and DFPP supplementary therapy. Although the level of interleukin-28B is an important predictor of a SVR, a decrease in the HCV RNA volume of ≥4 log IU/ml at week 2 after the initial treatment is also an important predictor. Therefore, rapid virological reduction using DFPP, in addition to IFN-β/RBV induction therapy, is an important predictor of a SVR.

Keywords: double filtration plasmapheresis; hepatitis C virus; interferon-β.