title: alpha-Interferon treatment of chronic hepatitis C in young patients with homozygous beta-thalassemia.
abstract: BACKGROUND
  Chronic infection with the hepatitis C virus (HCV) and iron overload are the main causes of chronic liver disease in subjects with homozygous beta-thalassemia (HBT). Iron overload can be counteracted by intensive chelation. alpha-interferon reduces viremia and necroinflammation in patients with chronic HCV hepatitis.
  
  
  METHODS
  To assess the effectiveness and safety of alpha 2b-Interferon (IFN), we enrolled in an open pilot trial of treatment 12 patients with HBT and biopsy-proven anti-HCV positive chronic hepatitis. IFN was given at a dose of 5 MU/m2 thrice weekly for 8 weeks, then 3 MU/m2 thrice weekly for 18 weeks. Patients were followed up to 24 months after stopping treatment when a second liver biopsy was performed in subjects with sustained response (normal ALT during follow-up).
  
  
  RESULTS
  Two patients discontinued IFN at 7 weeks because of haemolytic anemia and one after 8 weeks due to persistent fever. Among 9 subjects completing the protocol, 5 normalized ALT while on treatment and a further 2 within two months after stopping IFN. A sustained response was obtained altogether in 5 patients, since ALT relapsed in 2 responders. None of the 3 subjects who discontinued IFN and of the 2 patients who did not respond to treatment normalized ALT over a 24 months follow-up. Post-treatment liver histology in long-term responders showed a reduction of portal, periportal and lobular necroinflammation, while siderosis was essentially unchanged.
  
  
  CONCLUSIONS
  Although the pattern of response to IFN in HCV-infected subjects with HBT might differ from that of non-thalassemics, due to peculiar side effects and delayed response, the drug appears to be effective and deserves further investigation.
authors.affiliation: Istituto di Medicina Generale e Pneumologia, Università di Palermo, Italy.
authors.forename: V
authors.initials: V
authors.lastname: Di Marco
authors.forename: O
authors.initials: O
authors.lastname: Lo Iacono
authors.forename: M
authors.initials: M
authors.lastname: Capra
authors.forename: S
authors.initials: S
authors.lastname: Grutta
authors.forename: C
authors.initials: C
authors.lastname: Ciaccio
authors.forename: C
authors.initials: C
authors.lastname: Gerardi
authors.forename: A
authors.initials: A
authors.lastname: Maggio
authors.forename: D
authors.initials: D
authors.lastname: Renda
authors.forename: P
authors.initials: P
authors.lastname: Almasio
authors.forename: R
authors.initials: R
authors.lastname: Pisa
mesh_terms: D000293:Adolescent; D000410:Alanine Transaminase / Q000097:blood; D002648:Child; D005260:Female; D006432:Hemochromatosis / Q000150:complications; D006526:Hepatitis C / Q000150:complications / Q000473:pathology / Q000628:therapy*; D006521:Hepatitis, Chronic / Q000150:complications / Q000473:pathology / Q000628:therapy*; D006720:Homozygote; D006801:Humans; D007155:Immunologic Factors / Q000627:therapeutic use*; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D008297:Male; D011994:Recombinant Proteins; D012074:Remission Induction; D065227:Transfusion Reaction; D014766:Viremia / Q000150:complications / Q000628:therapy; D017086:beta-Thalassemia / Q000150:complications*
chemical_list: D007155:Immunologic Factors; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins; D000410:Alanine Transaminase