The database for this analysis includes clinical and demographic data extracted from the original database. To estimate the population frequency of the IL28B genotypes, 202 healthy volunteers with normal liver enzymes and no serological markers

of HCV, hepatitis B virus, human immunodeficiency virus, or other hepatic infection were also evaluated as a control population. These patients were all Caucasian and were recruited from the same geographical area. The study was approved by a central ethics committee and conducted in accordance with the provisions of the Declaration Roxadustat purchase of Helsinki and Good Clinical Practice guidelines. We selected the polymorphism rs12979860, located 3kB upstream of the IL28B gene,16, 18 for genotyping by the allele specific discrimination kit (ABI TaqMan) and the ABI 7900HT sequence detection System (Applied Biosystems). Genotyping was conducted in Italy, as previously reported,18 in a blinded fashion relative to HCV treatment status and other patient or treatment response characteristics. Genotyping calls were manually inspected and STA-9090 verified prior to release. Hardy-Weinberg Equilibrium was assessed. HCV

RNA levels were quantitatively measured by way of sensitive reverse-transcription polymerase chain reaction (Amplicor Monitor HCV 2.0; Roche Molecular Diagnostics, Basel, Switzerland) with a lower limit of detection of 600 IU/mL. Qualitative measurement of serum HCV RNA was performed at treatment weeks 0, 4, 8, 12, 24, and 48 and at follow-up evaluation at week 24. HCV RNA was qualitatively analyzed by way of polymerase chain reaction (Amplicor HCV; Roche Molecular Systems, Branchburg, NJ) with

a lower limit of detection of 50 IU/mL during and off therapy. HCV genotyping was performed by way of reverse 上海皓元医药股份有限公司 hybridization (INNO-LiPA HCV; Innogenetics, Gent, Belgium) in all patients. Histological results were classified by local pathologists following standard criteria according to Scheuer’s scoring system.19 Comparisons between groups were performed using a Wilcoxon test for nonnormal continuous variables. For categorical data, the Pearson χ2 test/Fisher exact test was used. P < 0.05 (two-sided) were regarded as significant. To determine the association of the IL28B single-nucleotide polymorphism with SVR in comparison with other predictors, we stratified each parameter as reported and analyzed them together with the ILB28 mutation in a forward conditional stepwise logistic regression model using SVR as the outcome variable. Results are presented as means and 95% confidence intervals (CIs) unless indicated otherwise. Covariates included in the model were baseline viral load (log10 IU/mL), liver fibrosis stage, inflammatory activity, sex, age, body mass index (BMI), serum alanine aminotransferase level, and IL28B genotype.