title: Changes in the acute phase complement component and IL-6 levels in patients with chronic hepatitis C receiving interferon alpha-2b.
abstract: In order to study the effect of interferon alpha on the levels of acute phase complement proteins in vivo, serum concentrations of C9 and C1-inhibitor (C1-INH) were measured in patients with chronic hepatitis C before and 3 months after the beginning of interferon alpha2b therapy. Serum levels of the activation product of terminal complement pathway, C5b-9, HCV RNA and IL-6 were also determined. IFN alpha treatment significantly (P<0.0001) increased the serum concentrations of both complement proteins. C5b-9 levels were found to significantly decrease during the same period of time. When the patients were divided into responders or non-responders (more or less than 50% decrease in plasma HCV RNA concentrations) C9 and C1-INH levels were elevated only in the responder patients. There was no correlation between the changes of IL-6 levels or the amounts of IFN alpha administrated on one hand, and the changes in the complement protein levels on the other. These findings suggest that the marked increase in the serum concentrations of the acute phase complement proteins is a secondary phenomenon due to the IFN alpha-caused diminution of the viral load and the resulting immune complex-induced complement activation.
authors.affiliation: National Institute of Haematology and Immunology, Budapest, Hungary.
authors.forename: L
authors.initials: L
authors.lastname: Bíró
authors.forename: L
authors.initials: L
authors.lastname: Varga
authors.forename: A
authors.initials: A
authors.lastname: Pár
authors.forename: E
authors.initials: E
authors.lastname: Nemesánszky
authors.forename: A
authors.initials: A
authors.lastname: Csepregi
authors.forename: L
authors.initials: L
authors.lastname: Telegdy
authors.forename: E
authors.initials: E
authors.lastname: Ibrányi
authors.forename: K
authors.initials: K
authors.lastname: Dávid
authors.forename: G
authors.initials: G
authors.lastname: Horváth
authors.forename: L
authors.initials: L
authors.lastname: Szentgyörgyi
authors.forename: I
authors.initials: I
authors.lastname: Nagy
authors.forename: L
authors.initials: L
authors.lastname: Dalmi
authors.forename: M
authors.initials: M
authors.lastname: Abonyi
authors.forename: G
authors.initials: G
authors.lastname: Füst
authors.forename: M
authors.initials: M
authors.lastname: Horányi
mesh_terms: D000209:Acute-Phase Proteins / Q000378:metabolism*; D000328:Adult; D003167:Complement Activation / Q000276:immunology; D003174:Complement C1 Inactivator Proteins / Q000378:metabolism; D003186:Complement C9 / Q000378:metabolism; D003165:Complement System Proteins / Q000378:metabolism*; D005260:Female; D016174:Hepacivirus / Q000276:immunology; D019698:Hepatitis C, Chronic / Q000097:blood / Q000276:immunology* / Q000628:therapy*; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000627:therapeutic use*; D015850:Interleukin-6 / Q000097:blood*; D008297:Male; D012367:RNA, Viral / Q000097:blood; D011994:Recombinant Proteins; D018709:Statistics, Nonparametric
chemical_list: D000209:Acute-Phase Proteins; D003174:Complement C1 Inactivator Proteins; D003186:Complement C9; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D015850:Interleukin-6; D012367:RNA, Viral; D011994:Recombinant Proteins; D003165:Complement System Proteins