This study aimed to investigate the prevalence of vitamin MK-2206 datasheet A deficiency among patients with chronic HCV infection and to assess whether vitamin A deficiency could be associated with unresponsiveness to interferon-based antiviral therapy. The analysis included 199 consecutive treatment-naïve chronic HCV patients in whom pretreatment serum vitamin A and 25-OH vitamin D were measured; 119 healthy blood donors were used as controls. Median (interquartile range) serum vitamin A in HCV-positive patients was significantly lower than in controls: 256 ng/mL (128-440) versus 742 (624-942, P < 0.0001). Overall sustained viral

response was achieved in 122/199 patients, 46/109 infected by difficult to treat HCV genotypes. In these latter, 39/104 (37.5%) were nonresponders. At multivariate analysis, nonresponse to antiviral therapy was predicted by carriage of interleukin (IL)-28B T/* genotypes, baseline serum levels of γGT >60 IU/mL, of HCV RNA >600,000 IU/mL, of vitamin A ≤100 ng/mL, and a cumulative dose of ribavirin ≤80%. Seventeen patients (9.0%) had both serum levels of vitamin A ≤100 ng/mL and of vitamin D ≤20 ng/mL; the presence PD-1 antibody inhibitor of a combined vitamin A and D deficiency was found to be a strong independent predictor of nonresponse to antiviral therapy. Conclusion: A high percentage of patients with chronic HCV infection

have serum vitamin A deficiency. This condition is associated with nonresponse to antiviral therapy. (HEPATOLOGY 2013) New specifically targeted direct antiviral agents (DAAs) against hepatitis C virus (HCV) have recently become available in many countries. However, they will not substitute, at least for several years, the interferon (IFN) plus ribavirin-based antiviral therapies. This is mainly due to the fact that although DAAs are very potent in inhibiting HCV replication, they are prone to favor the development of viral resistances if used in monotherapy. Triple antiviral therapy significantly improved the sustained viral response (SVR)

rates in HCV genotype 1 naïve-infected patients Tyrosine-protein kinase BLK compared to IFN plus ribavirin standard therapy. When treated with triple antiviral therapy, patients previously nonresponders to IFN plus ribavirin dual antiviral regimen achieved significantly lower SVR rates compared to relapsers.1, 2 The results suggest that the sensitivity of the host to the biological action of IFN is a prerequisite for the eradication of the infection, even using DAA triple therapy. Therefore, it would be important to understand if interferon sensitivity in the host could be modified prior to antiviral therapy in order to maximize the possibility to achieve SVR. Several not-modifiable and modifiable factors have been identified to help clinicians in predicting, prior to antiviral treatment and in individual patients, the probability of achieving SVR.