However, RBV-induced anemia is usually reversible and dose-related (7, 8). A new era was brought into being by the completion of the Human Genome Project, which included the genome-wide association study (GWAS). Imatinib PDGFR inhibitor According to several recent studies, genetic polymorphisms located near the interleukin 28B (IL28B) gene affect virologic response to treatment (9). In another study, polymorphisms of the inosine triphosphatase (ITPA) gene in chromosome 20 were found to influence RBV-induced anemia in CHC patients, and confirmed the presence of rs1127354 (a missense variants in exon 2) and rs7270101 (a splice-altering single nucleotide polymorphism [SNP] located in the second intron) (10). However, most research on this topic has been carried out in the USA and Europe.

In this study, the two main ITPA variants, which have been shown to be associated with RBV-induced anemia (rs1127354 and rs7270101) were investigated in Korean CHC patients treated with PEG-IFN plus RBV. In addition, we investigated the IL28B SNP, which has been shown to be most strongly associated with virologic response in genotype 1 patients. MATERIALS AND METHODS Patients enrollment In this retrospective cohort study, we studied 133 Korean patients with CHC infection treated at Gachon University Gil Medical Center from January 2008 to December 2011. Inclusion criteria were: 1) a diagnosis of CHC infection; 2) HCV genotype confirmed using the core region of HCV cDNA by polymerase chain reaction (PCR) and subsequent DNA sequencing; 3) a HCV RNA level of ��1,000 IU/mL determined by PCR using an Abbott m2000rt instrument (Abbott Laboratories, Chicago, IL) with a serum HCV RNA detection limit of <50 IU/mL; and 4) Korean ethnicity and an age from 20 to 70 yr.

Exclusion criteria were: 1) decompensated liver cirrhosis; 2) hepatitis B surface antigen positivity; 3) the presence or a history of hepatocellular carcinoma or 4) of other liver diseases, such as, autoimmune hepatitis, alcoholic liver disease, or a chronic liver disease other than CHC; 5) chronic renal disease, or 6) anemia before treatment (hemoglobin ��12 g/dL), absolute neutrophil count ��500 or thrombocytopenia (platelets ��100,000/��L). All patients were treated using a standard PEG-IFN alfa-2a plus RBV therapy. Patients with HCV genotype 1 were injected subcutaneously with 180 ��g of PEG-IFN alpha-2a (Pegasys?, F.

Hoffmann-La Roche, Ltd., Basel, Switzerland) per week regardless of weight plus 1,200 mg of RBV daily for patients >75 kg or 1,000 mg daily for patients <75 kg. Patients with HCV genotype 2 or 3 were treated with 180 ��g of PEG-IFN alfa-2a s.c. weekly and 800 mg of RBV daily. This standard combination therapy was continued for Brefeldin_A 48 weeks in patients with genotype 1 and for 24 weeks in patients with genotype 2 or 3.