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Serum B12 levels predict response to treatment with interferon and ribavirin in patients with chronic HCV infection
Author(s) -
Rosenberg P.,
Hagen K.
Publication year - 2011
Publication title -
journal of viral hepatitis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 100
eISSN - 1365-2893
pISSN - 1352-0504
DOI - 10.1111/j.1365-2893.2010.01288.x
Subject(s) - ribavirin , medicine , interferon , immunology , virology , chronic hepatitis , virus
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 p m in ETR and 260 p m in nonresponders (NR) ( P  = 0.012). In patients with s‐B12 levels ≤ 360 p m , 23 (31.5%) were NR and 50 (68.5%) had ETR. In patients with s‐B12 > 360 p m , 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 p m : 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 p m 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.

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