December 3, 2010

Vitamin D supplementation improves response to antiviral treatment for recurrent hepatitis C

Transplant International
Volume 24, Issue 1, pages 43–50, January 2011
DOI: 10.1111/j.1432-2277.2010.01141.x

Davide Bitetto 1, Carlo Fabris 1, Ezio Fornasiere 1, Corrado Pipan 2, Elisa Fumolo 1, Annarosa Cussigh 1, Sara Bignulin 1, Sara Cmet 1, Elisabetta Fontanini 1, Edmondo Falleti 1, Romina Martinella 2, Mario Pirisi 3,4, Pierluigi Toniutto 1

Author Information

1 Medical Liver Transplantation Unit, Internal Medicine, University of Udine, Udine, Italy
2 Hygiene and Epidemiology, University of Udine, Udine, Italy
3 Department of Clinical and Experimental Medicine, University of Eastern Piedmont “A. Avogadro”, Novara, Italy
4 Interdisciplinary Research Center of Autoimmune Diseases, University of Eastern Piedmont “A. Avogadro”, Novara, Italy

*Correspondence: Pierluigi Toniutto MD, DPMSC, Internal Medicine, Medical Liver Transplantation Unit, University of Udine, 33100 Udine, Italy. Tel.: +390432559801; fax: +39043242097; e-mail: pierluigi.toniutto@uniud.it

Abstract

Keywords: interferon; liver transplantation; recurrent hepatitis C; vitamin D

Summary

In immune-competent patients, higher vitamin D levels predicted sustained viral response (SVR) following interferon (INF) and ribavirin therapy for chronic hepatitis C. This study aimed to verify the influence of vitamin D serum levels and/or vitamin D supplementation in predicting SVR rates for recurrent hepatitis C (RHC). Forty-two consecutive patients were treated for RHC with combination therapy with INF-α and ribavirin for 48 weeks. Vitamin D serum levels were measured in all patients before antiviral therapy. In 15 patients oral vitamin D3 supplementation was administered to avoid further bone loss. SVR was observed in 13 patients; it was achieved in 1/10 severely vitamin D deficient (≤10 ng/ml) patients, in 6/20 deficient (>10 and ≤20 ng/ml) and in 6/12 with near normal (>20 ng/ml) 25-OH vitamin D serum levels (P < 0.05). Cholecalciferol supplementation, in the presence of a normal or near normal baseline vitamin D concentration, (improvement of chi-square P < 0.05, odds ratio 2.22) and possessing a genotype other than 1 (improvement of chi-square P < 0.05, odds ratio 3.383) were the only variables independently associated to SVR. In conclusion, vitamin D deficiency predicts an unfavourable response to antiviral treatment of RHC. Vitamin D supplementation improves the probability of achieving a SVR following antiviral treatment.

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