Document Detail

Reduced serum hepcidin levels in patients with chronic hepatitis C.
MedLine Citation:
PMID:  19729219     Owner:  NLM     Status:  MEDLINE    
BACKGROUND/AIMS: Patients with chronic hepatitis C (CHC) often have increased liver iron, a condition associated with reduced sustained response to antiviral therapy, more rapid progression to cirrhosis, and development of hepatocellular carcinoma. The hepatic hormone hepcidin is the major regulator of iron metabolism and inhibits iron absorption and recycling from erythrophagocytosis. Hepcidin decrease is a possible pathophysiological mechanism of iron overload in CHC, but studies in humans have been hampered so far by the lack of reliable quantitative assays for the 25-amino acid bioactive peptide in serum (s-hepcidin).
METHODS: Using a recently validated immunoassay, we measured s-hepcidin levels in 81 untreated CHC patients and 57 controls with rigorous definition of normal iron status. All CHC patients underwent liver biopsy with histological iron score.
RESULTS: s-hepcidin was significantly lower in CHC patients than in controls (geometric means with 95% confidence intervals: 33.7, 21.5-52.9 versus 90.9, 76.1-108.4 ng/mL, respectively; p<0.001). In CHC patients, s-hepcidin significantly correlated with serum ferritin and histological total iron score, but not with s-interleukin-6. After stratification for ferritin quartiles, s-hepcidin increased significantly across quartiles in both controls and CHC patients (chi for trend, p<0.001). However, in CHC patients, s-hepcidin was significantly lower than in controls for each corresponding quartile (analysis of variance, p<0.001).
CONCLUSIONS: These results, together with very recent studies in animal and cellular models, indicate that although hepcidin regulation by iron stores is maintained in CHC, the suppression of this hormone by hepatitis C virus is likely an important factor in liver iron accumulation in this condition.
Domenico Girelli; Michela Pasino; Julia B Goodnough; Elizabeta Nemeth; Maria Guido; Annalisa Castagna; Fabiana Busti; Natascia Campostrini; Nicola Martinelli; Italo Vantini; Roberto Corrocher; Tomas Ganz; Giovanna Fattovich
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-08-12
Journal Detail:
Title:  Journal of hepatology     Volume:  51     ISSN:  1600-0641     ISO Abbreviation:  J. Hepatol.     Publication Date:  2009 Nov 
Date Detail:
Created Date:  2009-10-14     Completed Date:  2010-02-02     Revised Date:  2014-09-14    
Medline Journal Info:
Nlm Unique ID:  8503886     Medline TA:  J Hepatol     Country:  England    
Other Details:
Languages:  eng     Pagination:  845-52     Citation Subset:  IM    
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MeSH Terms
Antimicrobial Cationic Peptides / blood*
Case-Control Studies
Ferritins / blood
Hepatitis C, Chronic / blood*,  complications,  metabolism,  virology
Iron / metabolism
Iron Overload / blood,  etiology,  metabolism
Middle Aged
Models, Biological
RNA, Viral / blood
Viral Load
Young Adult
Grant Support
F30 DK082151/DK/NIDDK NIH HHS; F30 DK082151-01/DK/NIDDK NIH HHS; GGP06213//Telethon; K01 DK075378/DK/NIDDK NIH HHS; K01 DK075378/DK/NIDDK NIH HHS; K01 DK075378-01/DK/NIDDK NIH HHS; R01 DK065029/DK/NIDDK NIH HHS; R01 DK065029/DK/NIDDK NIH HHS; R01 DK065029-01A1/DK/NIDDK NIH HHS
Reg. No./Substance:
0/Antimicrobial Cationic Peptides; 0/HAMP protein, human; 0/Hepcidins; 0/RNA, Viral; 0/hepcidin 25, human; 9007-73-2/Ferritins; E1UOL152H7/Iron

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