[27] Although treatment regimen or timing of virological evaluation differed in this and previous studies, the results were generally similar. Assessments of the associations between baseline IP-10 and other baseline clinical characteristics showed that IP-10 concentration correlated significantly with liver fibrosis and inflammation. IP-10

was significantly correlated with platelet count, reflecting fibrosis, and AST and ALT concentrations, reflecting inflammation. Furthermore, our AUC results showed that IP-10 levels were closely related to liver histological findings, confirming that IP-10 level is useful for predicting the extent of liver disease.[19, 20] Circulating IP-10 concentrations were found to correlate with intrahepatic levels of IP-10 mRNA.[22] Higher intrahepatic IP-10 mRNA may attract inflammatory cells into the liver, leading to the progression of liver fibrosis and inflammation. Higher circulating IP-10

selleck compound levels may result in the accumulation of effector T cells in the liver, with the selective pressure imposed by this accumulation Panobinostat chemical structure fostering the outgrowth of immune escape HCV mutants that are more difficult to eradicate with PEG IFN and RBV combination therapy.[17] It is of interest that age was almost significantly correlated with baseline IP-10 level in our study (rs = 0.200, P = 0.050). Asahina et al. demonstrated that advanced age was related to advanced liver histological findings.[35] Although a previous study reported significant differences in serum IP-10 concentrations between patients with different IL28B genotypes,[36] we did not observe similar findings. The reasons for these discrepancies are unclear, although they may have been due to racial differences. IP-10

concentrations were significantly lower in treatment-naïve than in relapsing patients and non-responders. This may have been due to the lower rates of F3/F4 liver fibrosis among treatment-naïve (21.1% [8/38]) than relapsing patients (24.2% [8/33]) and non-responders (42.9% [6/14]); and to the Aldehyde dehydrogenase lower rates of A2/A3 liver inflammation in treatment-naïve patients (42.1% [16/38]) than in relapsers (48.5% [16/33]) and non-responders (57.1% [8/14]). We found that RVR and SVR12 rates were comparable in patients with reduced initial TVR dose of 1500 mg/day and those with initial TVR dose of 2250 mg/day. Although investigating the impact of initial TVR dose on treatment outcomes was beyond the scope of this analysis, reduced initial dose of TVR may be as effective as the standard dose in some patients with HCV genotype 1. This study had several limitations, including its retrospective design and relatively small sample size. Moreover, treatment outcomes were missing for some patients, which may have introduced bias. Additionally, adherence to each study drug was not assessed, which may have also led to bias. Lastly, IFN-free regimens based on several DAA are expected to be approved in the near future.