Effect of iron depletion on serum markers of fibrogenesis, oxidative stress and serum liver enzymes in chronic hepatitis C: results of a pilot study
Article first published online: 19 FEB 2007
Volume 27, Issue 2, pages 268–273, March 2007
How to Cite
Alexander, J., Tung, B. Y., Croghan, A. and Kowdley, K. V. (2007), Effect of iron depletion on serum markers of fibrogenesis, oxidative stress and serum liver enzymes in chronic hepatitis C: results of a pilot study. Liver International, 27: 268–273. doi: 10.1111/j.1478-3231.2007.01449.x
- Issue published online: 19 FEB 2007
- Article first published online: 19 FEB 2007
- Received 6 July 2006accepted 8 November 2006
- hyaluronic acid;
- iron depletion;
- procollagen III peptide;
Background: Hepatic iron deposition has been associated with decreased response to interferon-α monotherapy, and has been speculated to contribute to disease progression in chronic hepatitis C (CHC). We performed this study to evaluate the effect of iron depletion on biochemical and virologic markers, and markers of lipid peroxidation and fibrogenesis.
Materials and Methods: Eighteen patients with CHC who did not have a virologic response to interferon monotherapy underwent weekly phlebotomies until iron depletion (serum ferritin <50 ng/ml). Serum levels of alanine transaminase (ALT), hepatitis C virus-RNA, transferrin saturation, ferritin, 8-isoprostane, hylauronic acid, amino-terminal procollagen III peptide and YKL-40 were measured before and after iron depletion.
Results: There was a statistically significant reduction of serum ALT, transferrin saturation and serum ferritin after iron depletion (range 4–11 phlebotomies). Serum ALT returned to normal after iron depletion in four (22%) patients. There was a significant reduction in serum procollagen III peptide level among patients who achieved biochemical response. No significant reduction was noted in serum levels of other markers.
Conclusions: Iron depletion was associated with a biochemical response in 22% of patients who did not respond to interferon monotherapy. There was a significant reduction in a key marker of fibrogenesis among patients with biochemical response. These data support longer-term studies of iron depletion in CHC.