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

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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.
Title: Impaired regulation of serum hepcidin during phlebotomy in patients with chronic hepatitis C
Description:
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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