Vitamin B12 supplementation improves rates of sustained viral response in patients chronically infected with hepatitis C virus

Gut2013;62:766-773 doi:10.1136/gutjnl-2012-302344

Hepatology

Original article 

Alba Rocco1, Debora Compare1, Pietro Coccoli1, Ciro Esposito2, Antimo Di Spirito2, Antonio Barbato3, Pasquale Strazzullo3, Gerardo Nardone1

+ Author Affiliations

Correspondence to Professor Gerardo Nardone, Department of Clinical and Experimental Medicine, Gastroenterology Unit, University of Naples “Federico II”, via Pansini 5, 80131 Naples, Italy; nardone@unina.it

Contributors AR, DC, GN: study concept and design and drafting of the manuscript. AR, DC, PC, CE, ADS: acquisition of data. AR, AB: analysis and interpretation of data; statistical analysis. PS, GN: critical revision of the manuscript for important intellectual content.

Revised 5 June 2012

Accepted 6 June 2012

Published Online First 17 July 2012

Abstract

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 naïve to antiviral therapy.

Methods Ninety-four patients with chronic HCV hepatitis were randomly assigned to receive pegylated interferon α plus ribavirin (standard-of-care; SOC) or SOC plus vitamin B₁₂ (SOC+B₁₂). Viral response—namely, 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-of-treatment 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 (p=0.03), end-of-treatment viral response (p=0.03) and SVR (p=0.001) 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 (p=0.002) and in patients with a high baseline viral load (p=0.002). Distribution of genotype IL-28B did not differ between the two groups. At multivariate analysis, only easy-to-treat HCV genotypes (OR=9.00; 95% CI 2.5 to 37.5; p=0.001) and vitamin B₁₂ supplementation (OR=6.9; 95% CI 2.0 to 23.6; p=0.002) were independently associated with SVR.

Conclusion Vitamin B₁₂ supplementation significantly improves SVR rates in HCV-infected patients naïve to antiviral therapy.

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