title: Two dose regimens of recombinant interferon-alpha-2b in chronic hepatitis C virus infection. Biochemistry, hepatitis C virus RNA, and liver histology as response indices.
abstract: BACKGROUND
  Recombinant interferon remains the cornerstone of treatment of chronic hepatitis C virus (HCV) infection. Still, evaluation of treatment on the basis of response indicators and long-term effect of the treatment raises several questions.
  
  
  METHODS
  Seventy-four patients with chronic HCV infection were randomized to a high (3 MIU, 3/7 days) or low (1 MIU, 3/7 days) dose of recombinant interferon-alpha-2b for 48 weeks after a 4-week course of 3 MIU, 3/7 days. Response to treatment was assessed by means of liver enzymes (transaminases), HCV RNA, and liver histology.
  
  
  RESULTS
  The higher maintenance dose was associated with a significantly higher rate of sustained alanine aminotransferase (ALAT) response (45% versus 19%) and with a significantly better chance of becoming HCV RNA-negative during therapy (47% versus 23%). In the high maintenance dose group 14 of the 29 (48%) patients with available HCV RNA data were negative at the 3-month follow-up, compared with 4 of 27 (15%) in the low maintenance dose group. Significantly more patients had improved liver biopsy findings after interferon in the high maintenance dose group (79%) than in the low maintenance dose group (36%). There was a close correlation between ALAT response and HCV RNA response. Of 17 patients who were HCV RNA-negative 3 months after the end of treatment, 10 remained HCV RNA-negative 2-4 years later.
  
  
  CONCLUSIONS
  The study demonstrates a higher response rate as assessed by biochemistry, HCV RNA, and liver histology in the higher dose group.
authors.affiliation: Medical Dept. A, Rikshospitalet, Oslo, Norway.
authors.forename: K
authors.initials: K
authors.lastname: Bjøro
authors.forename: H
authors.initials: H
authors.lastname: Krarup
authors.forename: H
authors.initials: H
authors.lastname: Bell
authors.forename: P
authors.initials: P
authors.lastname: Christophersen
authors.forename: S
authors.initials: S
authors.lastname: Evensen
authors.forename: S S
authors.initials: SS
authors.lastname: Frøland
authors.forename: A
authors.initials: A
authors.lastname: Laursen
authors.forename: B
authors.initials: B
authors.lastname: B vd Lippe
authors.forename: A
authors.initials: A
authors.lastname: Maeland
authors.forename: L
authors.initials: L
authors.lastname: Ranek
mesh_terms: D000328:Adult; D000368:Aged; D000998:Antiviral Agents / Q000008:administration & dosage*; D001483:Base Sequence; D002908:Chronic Disease; D004334:Drug Administration Schedule; D005260:Female; D005500:Follow-Up Studies; D016174:Hepacivirus / Q000235:genetics; D006526:Hepatitis C / Q000201:enzymology / Q000473:pathology / Q000628:therapy* / Q000821:virology; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000008:administration & dosage*; D008099:Liver / Q000473:pathology; D008297:Male; D008875:Middle Aged; D008969:Molecular Sequence Data; D012367:RNA, Viral / Q000032:analysis; D011994:Recombinant Proteins / Q000008:administration & dosage; D000637:Transaminases / Q000097:blood; D016896:Treatment Outcome
chemical_list: D000998:Antiviral Agents; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D012367:RNA, Viral; D011994:Recombinant Proteins; D000637:Transaminases