All laboratory tests were performed for each patient just before initiation of IFN therapy. Blood cell counts, serum alanine transaminase, gamma-glutamyl transpeptidase, hemoglobin A1c, total bilirubin, albumin, prothrombin time, and alpha-fetoprotein (AFP) were measured using commercially available assays. The HCV genotype was determined using polymerase chain reaction with the HCV Genotype Primer Kit (Institute of Immunology Co., Ltd., Tokyo, Japan) and classified as genotype 1, genotype 2, or other, according to Simmonds’ classification system. Serum HCV viral load

was determined using quantitative reverse transcription polymerase chain reaction using the COBAS TaqMan HCV Test (Roche Diagnostics, Branchburg, NJ, USA). The treatment protocol for CHC patients consisted of 1.5 μg/kg of pegylated RO4929097 manufacturer IFN-α-2b or 180 μg of pegylated IFN-α-2a once a week, combined with ribavirin at an oral dose of 600–1000 mg/day. Duration of the treatment was 48–72 weeks for those with HCV genotype 1 AZD2014 manufacturer and a serum HCV viral load > 5 log IU/mL. For all other patients, treatment lasted for 24 weeks. SVR was defined as undetectable serum HCV-RNA at 24 weeks after the end of treatment. Measurement of liver stiffness by transient elastography was performed using FibroScan (Echosens, Paris, France) within a week before treatment initiation. Technical

details of the examination and procedure have been reported previously.[17] Ten validated measurements were made on each patient, and results were expressed in kilopascals (kPa). Only procedures with 10 validated measurements and a success rate of at least 60% were considered reliable, and the median value was considered representative of the liver

elastic modulus. Serum AFP was measured every month, and ultrasonography or computed tomography were performed at least every 3–6 months for HCC surveillance during and after treatment, with a minimum follow-up duration of 6 months after the initiation of IFN therapy. HCC was diagnosed by histological examination and/or triphasic computerized tomography, in Mannose-binding protein-associated serine protease which hyperattenuation in the arterial phase with washout in the late phase is pathognomonic for HCC.[20] The status of patients enrolled in this study was confirmed as of March 2012. All analyses were conducted using IBM SPSS version 19 (IBM SPSS, Chicago, IL, USA), and P values less than 0.05 were considered statistically significant. Continuous variables and categorical variables were summarized as median (range) and percentage, respectively. Mann–Whitney U and chi-square tests were used when appropriate. The strength of the association between LSM and the histological fibrosis stage was estimated using the Spearman’s rank correlation coefficient.