title: Liver hepcidin mRNA correlates with iron stores, but not inflammation, in patients with chronic hepatitis C.
abstract: OBJECTIVE
  Liver iron is frequently elevated in chronic hepatitis C and may contribute to liver injury. The pathophysiology behind this phenomenon may involve hepcidin, a gene that is up-regulated in the liver by inflammation and iron. Inappropriately low hepcidin is important to the pathophysiology of hereditary hemochromatosis. However, the role of hepcidin in the iron loading of patients with hepatitis C is unknown.
  
  
  METHODS
  To determine whether liver hepcidin mRNA correlates with markers of hepatic inflammation and iron status in patients with hepatitis C, we extracted total RNA from liver biopsy specimens of patients with chronic hepatitis C and quantified hepcidin mRNA. Liver hepcidin mRNA levels were then correlated with aspartate aminotransferase, alanine aminotransferase, ferritin, viral load, fibrosis, hepatic iron concentration, and Hepatic Activity Index (HAI).
  
  
  RESULTS
  Among patients with hepatitis C, there was a significant correlation of hepcidin mRNA expression in the liver with hepatic iron concentration and serum ferritin (r = 0.72, P = 0.006, and r = 0.60, P = 0.01, respectively). Hepcidin mRNA expression in the liver did not correlate with aspartate aminotransferase, alanine aminotransferase, HAI, or viral load. No differences in hepcidin mRNA were found based on viral genotype or the presence of fibrosis.
  
  
  CONCLUSIONS
  In contrast to other inflammatory states, hepcidin mRNA expression in the liver was independent of markers of inflammation in hepatitis C. Instead, our results suggest that iron stores in patients with hepatitis C regulate hepcidin expression and that iron loading in chronic hepatitis C is not due to inappropriate hepcidin expression.
authors.affiliation: Department of Internal Medicine, University of California Davis Medical Center, Sacramento, CA 95817, USA.
authors.forename: Christopher A
authors.initials: CA
authors.lastname: Aoki
authors.forename: Lorenzo
authors.initials: L
authors.lastname: Rossaro
authors.forename: Rajendra
authors.initials: R
authors.lastname: Ramsamooj
authors.forename: David
authors.initials: D
authors.lastname: Brandhagen
authors.forename: Mary F
authors.initials: MF
authors.lastname: Burritt
authors.forename: Christopher L
authors.initials: CL
authors.lastname: Bowlus
mesh_terms: D000328:Adult; D000368:Aged; D023181:Antimicrobial Cationic Peptides / Q000235:genetics*; D005260:Female; D019698:Hepatitis C, Chronic / Q000235:genetics* / Q000276:immunology / Q000378:metabolism*; D064451:Hepcidins; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D007501:Iron / Q000378:metabolism*; D008099:Liver / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000096:biosynthesis*
chemical_list: D023181:Antimicrobial Cationic Peptides; C578702:HAMP protein, human; D064451:Hepcidins; D012333:RNA, Messenger; D007501:Iron