title: Effects of interferon therapy on fibrosis serum markers in HCV-positive chronic liver disease.
abstract: OBJECTIVE
  To evaluate serum levels of prolyl-hydroxylase and helical domain of Type IV collagen, markers of hepatic fibrogenesis, in patients with HCV-positive chronic liver disease and the effects of interferon therapy on these markers.
  
  
  METHODS
  Prolyl-hydroxylase and Type IV collagen were determined before therapy and each month during the treatment and follow-up.
  
  
  METHODS
  Fifty-seven HCV-positive patients were studied. All the subjects received alpha2a recombinant interferon, 6 MU subcutaneously three times a week for 4 weeks, followed by 3 MU thrice weekly for 5 months. After cessation of treatment, each patient was followed for 12 months. Prolyl-hydroxylase and helical domain of Type IV collagen were measured by using immunoenzymatic methods. HCV-RNA and HCV genotype were determined according to the method of Okamoto.
  
  
  RESULTS
  In the patients prolyl-hydroxylase (39.8+/-8.9 ng/ml) was not different from controls (39.1+/-5.9 ng/ml). On the contrary, the patients showed a mean Type IV collagen (133.6+/-93.3 ng/ml) significantly (P < 0.01) higher than controls (100.2+/-10.5 ng/ml). A good relationship between the degree of liver fibrosis and the Type IV collagen serum level was found (r = 0.68; P < 0.005). In both responders and non-responders the Type IV collagen levels decreased during interferon therapy. During the follow-up, in responders the Type IV collagen did not show modifications, while in non-responders/relapsers it returned rapidly to the pretreatment levels (139.1+/-100.7 ng/ml).
  
  
  CONCLUSIONS
  In HCV-positive chronic liver disease, prolylhydroxylase is not a good marker of hepatic fibrosis, while Type IV collagen is a useful tool for evaluating fibrogenic activity. Interferon seems to be able to reduce the liver fibrosis even without the inhibition of viral replication and independently from liver necrosis.
authors.affiliation: Istituto di Medicina Clinica, University School of Medicine, Trieste, Italy.
authors.forename: L
authors.initials: L
authors.lastname: Mazzoran
authors.forename: G
authors.initials: G
authors.lastname: Tamaro
authors.forename: M A
authors.initials: MA
authors.lastname: Mangiarotti
authors.forename: P
authors.initials: P
authors.lastname: Marchi
authors.forename: S
authors.initials: S
authors.lastname: Baracetti
authors.forename: U
authors.initials: U
authors.lastname: Gerini
authors.forename: M
authors.initials: M
authors.lastname: Fanni-Cannelles
authors.forename: F
authors.initials: F
authors.lastname: Zorat
authors.forename: G
authors.initials: G
authors.lastname: Pozzato
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015415:Biomarkers / Q000097:blood; D003094:Collagen / Q000097:blood*; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000302:isolation & purification; D006526:Hepatitis C / Q000097:blood* / Q000188:drug therapy; D006521:Hepatitis, Chronic / Q000097:blood / Q000188:drug therapy; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D008103:Liver Cirrhosis / Q000097:blood* / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D011393:Procollagen-Proline Dioxygenase / Q000097:blood*; D012367:RNA, Viral / Q000032:analysis; D011994:Recombinant Proteins
chemical_list: D015415:Biomarkers; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D012367:RNA, Viral; D011994:Recombinant Proteins; D003094:Collagen; D011393:Procollagen-Proline Dioxygenase