title: Clinical significance of elevated serum interferon- inducible protein-10 levels in hepatitis C virus carriers with persistently normal serum transaminase levels.
abstract: The aim of this study was to assess the immunological profile in hepatitis C virus carriers with persistently normal serum transaminase levels. Forty-two serum HCV RNA positive patients with persistently normal serum transaminase levels (22 natural 'asymptomatic HCV carriers' and 20 biochemical responders to IFN therapy) and 23 complete responders to IFN therapy were enrolled. The HCV genotypes and serum HCV RNA levels were determined before IFN therapy in treatment responders, and at entry in the others. The serum levels of IFN-inducible protein-10 (IP-10) (a protein mainly induced by IFN-gamma), interleukin (IL)-10, and IL-4 were measured in all patients while the serum transaminase levels were normal. The serum transaminase levels and platelet counts were then monitored for the next 4 years and the changes in liver fibrosis were assessed. The serum levels of IP-10 in infected and biochemically normal patients were significantly higher than the levels in complete responders to therapy, whereas the serum levels of IL-10 and IL-4 did not vary significantly among the different groups. During the 4-year follow-up period, 10/20 (50%) biochemical responders and 12/22 (55%) asymptomatic carriers had an elevation of the serum transaminase levels. A significant (P=0.0370) increase in platelet count after 4 years and improvement in liver fibrosis were noted in treatment responders but not in infected patients. The weak but significant residual immune response as reflected by the increased serum IP-10 level may underlie the outcome of HCV carriers with persistently normal serum transaminase levels.
authors.affiliation: Third Department of Internal Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan. yitoh@sun.kpu-m.ac.jp
authors.forename: Y
authors.initials: Y
authors.lastname: Itoh
authors.forename: A
authors.initials: A
authors.lastname: Morita
authors.forename: K
authors.initials: K
authors.lastname: Nishioji
authors.forename: S
authors.initials: S
authors.lastname: Narumi
authors.forename: T
authors.initials: T
authors.lastname: Toyama
authors.forename: Y
authors.initials: Y
authors.lastname: Daimon
authors.forename: H
authors.initials: H
authors.lastname: Nakamura
authors.forename: T
authors.initials: T
authors.lastname: Kirishima
authors.forename: T
authors.initials: T
authors.lastname: Okanoue
mesh_terms: D000410:Alanine Transaminase / Q000097:blood*; D000998:Antiviral Agents / Q000627:therapeutic use; D002353:Carrier State / Q000097:blood* / Q000188:drug therapy* / Q000201:enzymology / Q000473:pathology; D054357:Chemokine CXCL10; D019743:Chemokines, CXC / Q000097:blood*; D005260:Female; D005500:Follow-Up Studies; D016174:Hepacivirus / Q000235:genetics / Q000502:physiology; D006526:Hepatitis C / Q000097:blood* / Q000188:drug therapy* / Q000201:enzymology / Q000473:pathology; D006801:Humans; D016898:Interferon-alpha / Q000627:therapeutic use*; D016753:Interleukin-10 / Q000097:blood; D015847:Interleukin-4 / Q000097:blood; D008103:Liver Cirrhosis / Q000097:blood / Q000188:drug therapy / Q000201:enzymology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000097:blood / Q000235:genetics; D016896:Treatment Outcome; D019562:Viral Load
chemical_list: D000998:Antiviral Agents; D054357:Chemokine CXCL10; D019743:Chemokines, CXC; D016898:Interferon-alpha; D012367:RNA, Viral; D016753:Interleukin-10; D015847:Interleukin-4; D000410:Alanine Transaminase