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Published on: August 5, 2012
[Correlation of hepatic necrosis and complement system activation in fulminant viral hepatitis]
1Institute of Basic Medical Sciences, Beijing.
Insights
Complement activation causes liver damage in viral hepatitis. The C3d/C3 ratio indicates disease severity and may guide treatment for hepatic necrosis.
Area of Science:
- Immunology
- Hepatology
- Pathology
Context:
- Investigated the link between complement system activation and liver cell death (hepatic necrosis) in 110 patients with viral hepatitis.
- Analyzed plasma complement components (C3, C4) and their breakdown products (C3d, C4d), alongside liver tissue deposition of C3 and IgG in necrotic areas.
Purpose:
- To determine the role of complement activation in viral hepatitis-induced liver damage.
- To assess if complement activation markers correlate with disease severity and liver pathology.
Summary:
- Fulminant hepatitis showed excessive plasma C3 activation, with a higher C3d/C3 ratio correlating to clinical severity.
- Significant C3 and IgG deposition in necrotic liver tissue was observed in over 85% of fulminant hepatitis cases versus 37.5% in chronic active hepatitis.
Impact:
- Complement cascade activation is implicated as a driver of liver tissue damage in viral hepatitis.
- The C3d/C3 ratio may serve as a valuable biomarker for assessing hepatic pathology and guiding clinical management.
- Findings suggest potential new therapeutic strategies targeting the complement system.
Abstract:
The relationship between complement activation and hepatic necrosis was investigated in 110 cases of fulminant, acute or chronic viral hepatitis by examining plasma complement conversion products C3d and C4d and intact C3 and C4 molecules, as well as the local hepatic deposition of C3 IgG globulins in necrotic areas of the liver. The results revealed an excessive activation of plasma C3 in the fluminant hepatitis group. The C3d/C3 ratio was proved to be directly related to the severity of the clinical symptoms. C3 and IgG hepatic depositions in adjacent necrotic areas were found in over 85% of the fulminant hepatitis cases, as compared to 37.5% in cases of chronic active hepatitis. The conclusion was drawn that activation of the complement cascade is responsible for liver tissue damage, while the plasma complement activation represented by increased C3d and C3c fragment production might well reflect hepatic pathology. Therefore, the C3d/C3 ratio could serve as an index to aid clinical management, as well as pointing out a new therapeutic approach.
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