title: Patients with chronic hepatitis C achieving a sustained virological response to peginterferon and ribavirin therapy recover from impaired hepcidin secretion.
abstract: OBJECTIVE
  The aim of this study is to determine the clinical relevance of hepatic producing iron regulatory hormone-hepcidin, on iron overload in patients with chronic hepatitis C (CHC).
  
  
  METHODS
  Serum hepcidin was measured in 73 CHC patients by surface-enhanced laser desorption/ionization time of flight mass spectrometry (SELDI-TOF-MS), and compared to those of healthy controls and anemia of inflammation patients, and analyzed their relationship to hepatic hepcidin mRNA expression levels and clinical, hematological, and histological findings. The sequential changes of hepcidin were investigated in 27 CHC patients treated with a 48 week-course of pegylated-interferon (PEG-IFN) plus ribavirin therapy.
  
  
  RESULTS
  Serum hepcidin was positively correlated with hepatic hepcidin mRNA levels, serum ferritin and the degree of hepatic iron deposition in CHC. Serum hepcidin-to-ferritin ratios were significantly lower in HCV positive patients than in HCV negative controls in both hyper- and normal-ferritinemic conditions. This relative impairment of hepcidin production was fully reversible after successful HCV eradication by PEG-IFN plus ribavirin, concomitantly with the improvement of the iron overload condition.
  
  
  CONCLUSIONS
  The impairment of hepatic hepcidin production occurring with chronic HCV infection may enhance iron toxicity and lead to disease progression, and modulation or supplementation of hepcidin may be beneficial for these conditions in CHC.
authors.affiliation: Department of Gastroenterology and Hepatology, Division of Clinical Medicine and Biomedical Science, Institute of Medical Sciences, Mie University Graduate School of Medicine, Tsu, Mie 514-8507, Japan. nfujita@clin.medic.mie-u.ac.jp
authors.forename: Naoki
authors.initials: N
authors.lastname: Fujita
authors.forename: Ryosuke
authors.initials: R
authors.lastname: Sugimoto
authors.forename: Satoshi
authors.initials: S
authors.lastname: Motonishi
authors.forename: Naohisa
authors.initials: N
authors.lastname: Tomosugi
authors.forename: Hideaki
authors.initials: H
authors.lastname: Tanaka
authors.forename: Masaki
authors.initials: M
authors.lastname: Takeo
authors.forename: Motoh
authors.initials: M
authors.lastname: Iwasa
authors.forename: Yoshinao
authors.initials: Y
authors.lastname: Kobayashi
authors.forename: Hisao
authors.initials: H
authors.lastname: Hayashi
authors.forename: Masahiko
authors.initials: M
authors.lastname: Kaito
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Takei
mesh_terms: D000328:Adult; D000368:Aged; D023181:Antimicrobial Cationic Peptides / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D000998:Antiviral Agents / Q000008:administration & dosage*; D016022:Case-Control Studies; D004359:Drug Therapy, Combination; D005260:Female; D005293:Ferritins / Q000097:blood; D019698:Hepatitis C, Chronic / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology* / Q000821:virology; D064451:Hepcidins; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000008:administration & dosage*; D019190:Iron Overload / Q000150:complications / Q000503:physiopathology; D008099:Liver / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011092:Polyethylene Glycols; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011994:Recombinant Proteins; D012254:Ribavirin / Q000008:administration & dosage*
chemical_list: D023181:Antimicrobial Cationic Peptides; D000998:Antiviral Agents; C578702:HAMP protein, human; D064451:Hepcidins; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D012333:RNA, Messenger; D011994:Recombinant Proteins; D011092:Polyethylene Glycols; D012254:Ribavirin; D005293:Ferritins; C417083:peginterferon alfa-2b