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Complement activation correlates with liver necrosis and fibrosis in chronic hepatitis C

MPG-Autoren
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Vasel,  Matthäus
Nakchbandi, Inaam / Translational Medicine, Max Planck Institute of Biochemistry, Max Planck Society;

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Nakchbandi,  Inaam A.
Nakchbandi, Inaam / Translational Medicine, Max Planck Institute of Biochemistry, Max Planck Society;

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Zitation

Vasel, M., Rutz, R., Bersch, C., Feick, P., Singer, M. V., Kirschfink, M., et al. (2014). Complement activation correlates with liver necrosis and fibrosis in chronic hepatitis C. CLINICAL IMMUNOLOGY, 150(2), 149-156. doi:10.1016/j.clim.2013.11.014.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-0018-F00B-D
Zusammenfassung
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. (C) 2013 Elsevier Inc. All rights reserved.