title: Complement activation correlates with liver necrosis and fibrosis in chronic hepatitis C.
abstract: Chronic hepatitis C viral infection modulates complement. The aim of this study was to determine whether complement analysis predicts liver inflammation and fibrosis in patients with chronic hepatitis C. 50 chronic hepatitis C patients who underwent a liver biopsy were compared to 50 healthy controls and 35 patients with various liver diseases. Total plasma complement activity (CH50) in plasma was diminished in hepatitis C patients suggesting complement activation. This decrease correlated with increased necrosis (r = -0.24, p < 0.05), and patients with levels below the normal range had a higher METAVIR activity score reflecting enhanced inflammation. SC5b-9, a marker of complement activation, correlated with inflammation (r = 0.40, p < 0.05), activity (r = 0.42, p < 0.05), and fibrosis scores (r = 0.49, p < 0.05). Finally, the prevalence of C1q auto-antibodies was higher in hepatitis C patients, and their presence was associated with increased inflammation and seemed to affect fibrosis. We conclude that complement-induced liver inflammation contributes to fibrosis in patients with chronic hepatitis C.
authors.affiliation: Max-Planck Institute of Biochemistry, Martinsried, Germany; Institute of Immunology, University of Heidelberg, Germany.
authors.forename: Matthäus
authors.initials: M
authors.lastname: Vasel
authors.affiliation: Institute of Immunology, University of Heidelberg, Germany.
authors.forename: Renate
authors.initials: R
authors.lastname: Rutz
authors.affiliation: Institute for Pathology, University of Heidelberg at Mannheim, Germany.
authors.forename: Claus
authors.initials: C
authors.lastname: Bersch
authors.affiliation: Department of Medicine II, University of Heidelberg at Mannheim, Germany.
authors.forename: Peter
authors.initials: P
authors.lastname: Feick
authors.affiliation: Department of Medicine II, University of Heidelberg at Mannheim, Germany.
authors.forename: Manfred V
authors.initials: MV
authors.lastname: Singer
authors.affiliation: Institute of Immunology, University of Heidelberg, Germany.
authors.forename: Michael
authors.initials: M
authors.lastname: Kirschfink
authors.affiliation: Max-Planck Institute of Biochemistry, Martinsried, Germany; Institute of Immunology, University of Heidelberg, Germany. Electronic address: inaam.nakchbandi@immu.uni-heidelberg.de.
authors.forename: Inaam A
authors.initials: IA
authors.lastname: Nakchbandi
mesh_terms: D000328:Adult; D001323:Autoantibodies / Q000276:immunology; D015415:Biomarkers / Q000378:metabolism; D003167:Complement Activation / Q000276:immunology*; D015922:Complement C1q / Q000276:immunology; D003165:Complement System Proteins / Q000276:immunology / Q000378:metabolism; D005260:Female; D005353:Fibronectins / Q000378:metabolism; D019698:Hepatitis C, Chronic / Q000150:complications / Q000175:diagnosis / Q000276:immunology* / Q000473:pathology*; D006801:Humans; D008099:Liver / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008103:Liver Cirrhosis / Q000150:complications / Q000175:diagnosis / Q000276:immunology* / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D009336:Necrosis; D011379:Prognosis
chemical_list: D001323:Autoantibodies; D015415:Biomarkers; D005353:Fibronectins; D015922:Complement C1q; D003165:Complement System Proteins
keywords: Chronic hepatitis C;; Complement;; Fibronectin; Fibrosis;; Inflammation;; Stellate cell;