Volume 39, Issue 6 pp. 619-624

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

Ryosuke Sugimoto

Ryosuke Sugimoto

Department of Gastroenterology and Hepatology, Division of Clinical Medicine and Biomedical Science, Institute of Medical Sciences, Mie University Graduate School of Medicine, Mie, and

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Naoki Fujita

Corresponding Author

Naoki Fujita

Department of Gastroenterology and Hepatology, Division of Clinical Medicine and Biomedical Science, Institute of Medical Sciences, Mie University Graduate School of Medicine, Mie, and

Dr Naoki Fujita, Department of Gastroenterology and Hepatology, Division of Clinical Medicine and Biomedical Science, Institute of Medical Sciences, Mie University Graduate School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan. Email: [email protected]Search for more papers by this author
Naohisa Tomosugi

Naohisa Tomosugi

Division of Clinical Science, Medical Research Institute, Kanazawa Medical University, Kanzawa, Japan

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Nagisa Hara

Nagisa Hara

Department of Gastroenterology and Hepatology, Division of Clinical Medicine and Biomedical Science, Institute of Medical Sciences, Mie University Graduate School of Medicine, Mie, and

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Hirohide Miyachi

Hirohide Miyachi

Department of Gastroenterology and Hepatology, Division of Clinical Medicine and Biomedical Science, Institute of Medical Sciences, Mie University Graduate School of Medicine, Mie, and

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Hideaki Tanaka

Hideaki Tanaka

Department of Gastroenterology and Hepatology, Division of Clinical Medicine and Biomedical Science, Institute of Medical Sciences, Mie University Graduate School of Medicine, Mie, and

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Masaki Takeo

Masaki Takeo

Department of Gastroenterology and Hepatology, Division of Clinical Medicine and Biomedical Science, Institute of Medical Sciences, Mie University Graduate School of Medicine, Mie, and

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Naoki Nakagawa

Naoki Nakagawa

Department of Gastroenterology and Hepatology, Division of Clinical Medicine and Biomedical Science, Institute of Medical Sciences, Mie University Graduate School of Medicine, Mie, and

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Motoh Iwasa

Motoh Iwasa

Department of Gastroenterology and Hepatology, Division of Clinical Medicine and Biomedical Science, Institute of Medical Sciences, Mie University Graduate School of Medicine, Mie, and

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Yoshinao Kobayashi

Yoshinao Kobayashi

Department of Gastroenterology and Hepatology, Division of Clinical Medicine and Biomedical Science, Institute of Medical Sciences, Mie University Graduate School of Medicine, Mie, and

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Masahiko Kaito

Masahiko Kaito

Department of Gastroenterology and Hepatology, Division of Clinical Medicine and Biomedical Science, Institute of Medical Sciences, Mie University Graduate School of Medicine, Mie, and

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Yoshiyuki Takei

Yoshiyuki Takei

Department of Gastroenterology and Hepatology, Division of Clinical Medicine and Biomedical Science, Institute of Medical Sciences, Mie University Graduate School of Medicine, Mie, and

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First published: 22 May 2009
Citations: 10

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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