Vitamin B12 supplementation improves rates ofsustained viral response in patients chronicallyinfected with hepatitis C virus

Background In vitro, vitamin B12 acts as a natural inhibitor of hepatitis C virus (HCV) replication. Objective To assess the effect of vitamin B12 on virological response in patients with chronic HCV hepatitis naı ¨ve to antiviral therapy. Methods Ninety-four patients with chronic HCV hepatitis were randomly assigned to receive pegylated interferon a plus ribavirin (standard-of-care; SOC) or SOC plus vitamin B12 (SOC+B12). Viral responsednamely, undetectable serum HCV-RNA, was evaluated 4 weeks after starting treatment (rapid viral response), 12 weeks after starting treatment (complete early viral response) and 24 or 48 weeks after starting treatment (end-oftreatment viral response) and 24 weeks after completing treatment (sustained viral response (SVR)). Genotyping for the interleukin (IL)-28B polymorphism was performed a posteriori in a subset (42/64) of HCV genotype 1 carriers. Results Overall, rapid viral response did not differ between the two groups, whereas the rates of complete early viral response (p¼0.03), end-of-treatment viral response (p¼0.03) and SVR (p¼0.001) were significantly higher in SOC+B12 patients than in SOC patients. In SOC+B12 patients, the SVR rate was also significantly higher in carriers of a difficult-to-treat genotype (p¼0.002) and in patients with a high baseline viral load (p¼0.002). Distribution of genotype IL-28B did not differ between the two groups. At multivariate analysis, only easy-to-treat HCV genotypes (OR¼9.00; 95% CI 2.5 to 37.5; p¼0.001) and vitamin B12 supplementation (OR¼6.9; 95% CI 2.0 to 23.6; p¼0.002) were independently associated with SVR. Conclusion Vitamin B12 supplementation significantly improves SVR rates in HCV-infected patients naı ¨ve to antiviral therapy.