2009•Hepatology ResearchRequires access

Impaired regulation of serum hepcidin during phlebotomy in patients with chronic hepatitis C

Ryosuke Sugimoto, Naoki Fujita, Naohisa Tomosugi, Nagisa Hara, Hirohide Miyachi, Hideaki Tanaka, Masaki Takeo, Naoki Nakagawa, Motoh Iwasa, Yoshinao Kobayashi, Masahiko Kaito, Yoshiyuki Takei

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Abstract

AIM: This study was conducted to determine the clinical relevance of hepcidin, a recently identified key iron regulatory hormone, in patients with chronic hepatitis C virus (C-HCV). METHODS: Serum hepcidin levels were measured in 9 C-HCV patients by surface-enhanced laser desorption/ionization time of flight mass spectrometry (SELDI-TOF-MS), and compared to those of healthy controls. Sequential changes of hepcidin were also investigated during phlebotomy. RESULTS: Serum hepcidin and ferritin were significantly higher in C-HCV than in controls (P = 0.0002), these two variables were strongly related to each other (r = 0.658; P < 0.01), and phlebotomy significantly decreased serum hepcidin in C-HCV (P = 0.0007); all these results recollect the hepcidin response to iron signal. Hepcidin/ferritin ratio, an index of the appropriateness of hepcidin expression relative to iron overload, was significantly lower in C-HCV than in controls (0.33 +/- 0.41 vs. 0.73 +/- 0.36, P = 0.0068). This relative impairment of hepcidin expression was not reversible after phlebotomy (P = NS). CONCLUSIONS: Although the hepcidin expression responds to iron conditions in C-HCV, this response is relatively limited. This relative impairment of hepcidin expression may be relevant to disease progression, and thus correction of its regulation may be beneficial for these iron-overloaded C-HCV patients.

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What this paper is about

AIM: This study was conducted to determine the clinical relevance of hepcidin, a recently identified key iron regulatory hormone, in patients with chronic hepatitis C virus (C-HCV). METHODS: Serum hepcidin levels were measured in 9 C-HCV patients by surface-enhanced laser desorption/ionization time of flight mass spectrometry (SELDI-TOF-MS), and compared to those of healthy controls. Sequential changes of hepcidin were also investigated during phlebotomy. RESULTS: Serum hepcidin and ferritin were significantly higher in C-HCV than in controls (P = 0.0002), these two variables were strongly related to each other (r = 0.658; P < 0.01), and phlebotomy significantly decreased serum hepcidin in C-HCV (P = 0.0007); all these results recollect the hepcidin response to iron signal. Hepcidin/ferritin ratio, an index of the appropriateness of hepcidin expression relative to iron overload, was significantly lower in C-HCV than in controls (0.33 +/- 0.41 vs. 0.73 +/- 0.36, P = 0.0068). This relative impairment of hepcidin expression was not reversible after phlebotomy (P = NS). CONCLUSIONS: Although the hepcidin expression responds to iron conditions in C-HCV, this response is relatively limited. This relative impairment of hepcidin expression may be relevant to disease progression, and thus correction of its regulation may be beneficial for these iron-overloaded C-HCV patients.

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Available abstract

AIM: This study was conducted to determine the clinical relevance of hepcidin, a recently identified key iron regulatory hormone, in patients with chronic hepatitis C virus (C-HCV). METHODS: Serum hepcidin levels were measured in 9 C-HCV patients by surface-enhanced laser desorption/ionization time of flight mass spectrometry (SELDI-TOF-MS), and compared to those of healthy controls. Sequential changes of hepcidin were also investigated during phlebotomy. RESULTS: Serum hepcidin and ferritin were significantly higher in C-HCV than in controls (P = 0.0002), these two variables were strongly related to each other (r = 0.658; P < 0.01), and phlebotomy significantly decreased serum hepcidin in C-HCV (P = 0.0007); all these results recollect the hepcidin response to iron signal. Hepcidin/ferritin ratio, an index of the appropriateness of hepcidin expression relative to iron overload, was significantly lower in C-HCV than in controls (0.33 +/- 0.41 vs. 0.73 +/- 0.36, P = 0.0068). This relative impairment of hepcidin expression was not reversible after phlebotomy (P = NS). CONCLUSIONS: Although the hepcidin expression responds to iron conditions in C-HCV, this response is relatively limited. This relative impairment of hepcidin expression may be relevant to disease progression, and thus correction of its regulation may be beneficial for these iron-overloaded C-HCV patients.

Key concepts: Hepcidin, Phlebotomy, Ferritin, Medicine, Internal medicine, Endocrinology, Chronic hepatitis, Immunology

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