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

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Journal of Viral Hepatitis

Here is an interesting article.

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

P. Rosenberg, K. Hagen
Journal of Viral Hepatitis: Volume 18,Issue 2, pages 129-134 February 2011

Summary

Background and Aim

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.

Patients and Methods

Ninety-nine treatment naive 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.

Results

  • Mean pretreatment s-B12 was 331pm in ETR and 260 pm in nonresponders (NR) (P< =0.012).
  • In patients with s-B12 levels less than 360 pm, 23 (31.5%) were NR and 50 (68.5%) had ETR.
  • In patients with s-B12 more than 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.