title: Raised serum ferritin predicts non-response to interferon and ribavirin treatment in patients with chronic hepatitis C infection.
abstract: OBJECTIVE
  Previous studies have indicated that response to interferon therapy is inversely proportional to the amount of body iron stores. We have studied the relationship between serum ferritin, transferrin saturation, liver iron, presence of HFE-C282Y gene mutation and response to treatment in patients with chronic hepatitis C infection.
  
  
  METHODS
  Two hundred and fifty-six naive, HCV-RNA positive patients (60% males, median age 38 years, range 21-70) were treated with interferon and ribavirin for 6 months. Iron indices and the presence of the C282Y mutation were measured. In 242 (94%) patients iron deposition were determined by Perls staining method. Patients with negative HCV-RNA at 6 months after the end of treatment were defined as sustained viral responders.
  
  
  RESULTS
  Non-responders (n = 127) had significantly higher median s-ferritin values compared with sustained viral responders (130 microg/L vs. 75 microg/L P < 0.001). There was no difference in transferrin saturation among the two response groups. Only 23% (4/7) of patients with Perls grade 1 in liver biopsies responded to treatment vs. 54% (122/225) patients without iron deposition (P = 0.02), however, 10/13-non-responders had HCV genotype one. Two patients (0.8%) were homozygous for the C282Y mutation, 36 patients were heterozygous (14%). Among mutation carriers 26/38 achieved sustained response compared with 102/216 non-carriers (68% vs. 48%, P = 0.02). In a multivariate analysis s-ferritin (P = 0.030) and C282Y carrier status (P = 0.012) remained independent predict of sustained response.
  
  
  CONCLUSIONS
  Raised s-ferritin values predicate non-response to interferon-ribavirin therapy in hepatitis C patients. Response rate in C282Y mutation carriers seems greater than in non-carriers.
authors.affiliation: Hepatology Unit, Department of Medicine, Aker University Hospital, Oslo, Norway. sonia.distante@ioks.uio.no
authors.forename: S
authors.initials: S
authors.lastname: Distante
authors.forename: K
authors.initials: K
authors.lastname: Bjøro
authors.forename: K B
authors.initials: KB
authors.lastname: Hellum
authors.forename: B
authors.initials: B
authors.lastname: Myrvang
authors.forename: J P
authors.initials: JP
authors.lastname: Berg
authors.forename: K
authors.initials: K
authors.lastname: Skaug
authors.forename: N
authors.initials: N
authors.lastname: Raknerud
authors.forename: H
authors.initials: H
authors.lastname: Bell
mesh_terms: D000328:Adult; D000368:Aged; D000998:Antiviral Agents / Q000627:therapeutic use*; D004359:Drug Therapy, Combination; D005260:Female; D005293:Ferritins / Q000097:blood*; D005838:Genotype; D000071020:Hemochromatosis Protein; D016174:Hepacivirus / Q000235:genetics / Q000302:isolation & purification; D019698:Hepatitis C, Chronic / Q000097:blood / Q000188:drug therapy* / Q000235:genetics; D015395:Histocompatibility Antigens Class I / Q000235:genetics; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use*; D007501:Iron / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008297:Male; D008565:Membrane Proteins / Q000235:genetics; D008875:Middle Aged; D009154:Mutation; D012367:RNA, Viral / Q000097:blood; D012254:Ribavirin / Q000627:therapeutic use*; D016896:Treatment Outcome; D019562:Viral Load
chemical_list: D000998:Antiviral Agents; C103673:HFE protein, human; D000071020:Hemochromatosis Protein; D015395:Histocompatibility Antigens Class I; D016898:Interferon-alpha; D008565:Membrane Proteins; D012367:RNA, Viral; D012254:Ribavirin; D005293:Ferritins; D007501:Iron