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Vitamin B12 supplementation improves rates of sustained viral response in patients chronically infected with hepatitis C virus
  1. Alba Rocco1,
  2. Debora Compare1,
  3. Pietro Coccoli1,
  4. Ciro Esposito2,
  5. Antimo Di Spirito2,
  6. Antonio Barbato3,
  7. Pasquale Strazzullo3,
  8. Gerardo Nardone1
  1. 1Department of Clinical and Experimental Medicine, Gastroenterology Unit, University of Naples “Federico II”, Naples, Italy
  2. 2Unit of Virology, “D. Cotugno” Hospital, Naples, Italy
  3. 3Internal Medicine Unit, University of Naples “Federico II”, Naples, Italy
  1. 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{at}unina.it

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.

  • Vitamin B12
  • chronic hepatitis C
  • interferon
  • ribavirin
  • response to treatment
  • 13C-urea breath test
  • angiodysplasia
  • breath tests
  • celiac disease
  • gastric adenocarcinoma
  • helicobacter pylori
  • pathogenesis
  • gastric metaplasia
  • gastric cancer
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Footnotes

  • Competing interests None.

  • Ethics approval Ethical Committee University Federico II of Naples.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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