Serum B12 levels predict response to treatment with interferon and ribavirin in patients with chronic HCV infection

[Guest guest]

http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2893.2010.01288.x/abstract

Serum B12 levels predict response to treatment with interferon and ribavirin in

patients with chronic HCV infection

P. Rosenberg1,2, K. Hagen2Article first published online: 19 FEB 2010

DOI: 10.1111/j.1365-2893.2010.01288.x

© 2010 Blackwell Publishing Ltd

Issue

Journal of Viral Hepatitis

Volume 18, Issue 2, pages 129–134, February 2011

Summary.  Vitamin B12 is stored in hepatocytes and inhibits hepatitis C virus

(HCV) RNA translation. The implication of B12 in the setting of antiviral

treatment is unknown. This study aims to retrospectively evaluate the

discriminative efficacy of pretreatment B12 serum levels (s-B12) on

end-of-treatment response (ETR) in patients with chronic HCV. Ninety-nine

treatment naïve HCV patients, treated with interferon and ribavirin were

studied. Serum B12 (s-B12) was analysed in samples collected before treatment

start. Pretreatment s-B12 levels were correlated to ETR using univariate

analysis. S-B12 and clinical data were evaluated in a multivariate logistic

regression model. Mean pretreatment s-B12 was 331 pm in ETR and 260 pm in

nonresponders (NR) (P = 0.012). In patients with s-B12 levels ≤ 360 pm, 23

(31.5%) were NR and 50 (68.5%) had ETR. In patients with s-B12 > 360 pm, one

(3.8%) was NR and 25 (96.2%) had ETR (P = 0.0034). The results of the

multivariate analysis were as follows: Pretreatment s-B12 > 360 vs≤360 pm: OR

28.6 CI 2.31–354, P = 0.008. Fibrosis stage 3–4 vs 0–2: OR 0.29 CI

0.074–1.12, P = 0.068. Genotype 2/3 vs 1/4/5: OR 15.5 CI 2.87–83.9, P =

0.0012. Dose reduction vs no dose reduction: OR 0.21, CI 0.048–0.91 P = 0.034.

Standard interferon vs pegylated-interferon: OR 0.079, CI 0.0091–0.68 P =

0.019. Age and gender were not correlated to ETR. S-B12 > 360 pm is

independently correlated to ETR in HCV patients treated with interferon and

ribavirin. This suggests that B12 is involved in suppression of viral

replication during anti-HCV treatment.

[Guest guest]

http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2893.2010.01288.x/abstract

Serum B12 levels predict response to treatment with interferon and ribavirin in

patients with chronic HCV infection

P. Rosenberg1,2, K. Hagen2Article first published online: 19 FEB 2010

DOI: 10.1111/j.1365-2893.2010.01288.x

© 2010 Blackwell Publishing Ltd

Issue

Journal of Viral Hepatitis

Volume 18, Issue 2, pages 129–134, February 2011

Summary.  Vitamin B12 is stored in hepatocytes and inhibits hepatitis C virus

(HCV) RNA translation. The implication of B12 in the setting of antiviral

treatment is unknown. This study aims to retrospectively evaluate the

discriminative efficacy of pretreatment B12 serum levels (s-B12) on

end-of-treatment response (ETR) in patients with chronic HCV. Ninety-nine

treatment naïve HCV patients, treated with interferon and ribavirin were

studied. Serum B12 (s-B12) was analysed in samples collected before treatment

start. Pretreatment s-B12 levels were correlated to ETR using univariate

analysis. S-B12 and clinical data were evaluated in a multivariate logistic

regression model. Mean pretreatment s-B12 was 331 pm in ETR and 260 pm in

nonresponders (NR) (P = 0.012). In patients with s-B12 levels ≤ 360 pm, 23

(31.5%) were NR and 50 (68.5%) had ETR. In patients with s-B12 > 360 pm, one

(3.8%) was NR and 25 (96.2%) had ETR (P = 0.0034). The results of the

multivariate analysis were as follows: Pretreatment s-B12 > 360 vs≤360 pm: OR

28.6 CI 2.31–354, P = 0.008. Fibrosis stage 3–4 vs 0–2: OR 0.29 CI

0.074–1.12, P = 0.068. Genotype 2/3 vs 1/4/5: OR 15.5 CI 2.87–83.9, P =

0.0012. Dose reduction vs no dose reduction: OR 0.21, CI 0.048–0.91 P = 0.034.

Standard interferon vs pegylated-interferon: OR 0.079, CI 0.0091–0.68 P =

0.019. Age and gender were not correlated to ETR. S-B12 > 360 pm is

independently correlated to ETR in HCV patients treated with interferon and

ribavirin. This suggests that B12 is involved in suppression of viral

replication during anti-HCV treatment.