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Effect of iron depletion on serum markers of fibrogenesis, oxidative stress and serum liver enzymes in chronic hepatitis C: results of a pilot study
Author(s) -
Alexander Jacob,
Tung Bruce Y.,
Croghan Anne,
Kowdley Kris V.
Publication year - 2007
Publication title -
liver international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.873
H-Index - 110
eISSN - 1478-3231
pISSN - 1478-3223
DOI - 10.1111/j.1478-3231.2007.01449.x
Subject(s) - oxidative stress , chronic hepatitis , medicine , enzyme , liver enzyme , hepatitis , gastroenterology , immunology , chemistry , biochemistry , virus
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.