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Detection and characterization of circulating immune complexes during acute exacerbation of chronic viral hepatitis
Insights
Circulating immune complexes (CIC) are elevated in liver disease patients, unlike asymptomatic carriers. These complexes, including Hepatitis B surface antigen (HBsAg) and IgG, change during disease exacerbation.
Area of Science:
- Immunology
- Hepatology
- Biochemistry
Background:
- Circulating immune complexes (CIC) play a role in various immune-mediated diseases.
- Liver diseases are often associated with immune system dysregulation.
- Understanding CIC composition and behavior is crucial for diagnosis and management.
Purpose of the Study:
- To detect and characterize CIC in patients with different liver diseases.
- To investigate the relationship between CIC levels and disease activity.
- To identify components of CIC in Hepatitis B virus (HBV)-related liver disease.
Main Methods:
- C1q binding test (C1q BT) for CIC detection.
- Analysis of CIC sedimentation rates.
- Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) for component analysis.
Main Results:
- CIC levels were significantly higher in liver disease patients compared to asymptomatic HBsAg carriers.
- Two distinct CIC sizes were observed based on sedimentation rates.
- CIC levels peaked 1-5 weeks relative to sGPT peaks during acute exacerbations.
- SDS-PAGE revealed HBsAg and IgG as components of CIC in severe chronic active hepatitis, with consistent HBsAg presence during exacerbations.
Conclusions:
- C1q BT is effective for detecting CIC in liver diseases.
- CIC levels and composition vary with liver disease type and activity.
- HBsAg is a significant component of CIC in some HBV-related liver diseases, correlating with disease activity.
Abstract:
For detection and characterization of circulating immune complexes (CIC) in various liver diseases, a C1q binding test (C1q BT) was used. While the CIC level was almost normal in HB surface antigen (HBsAg) positive asymptomatic carriers, it was relatively high in patients with liver diseases. The study of the sedimentation rate of CIC in various liver diseases showed two kinds of CIC; one greater than the other. During acute exacerbation of chronic active liver diseases, the CIC level reached its peak 1-5 weeks before and after the peak of sGPT. In acid buffer, CIC in one patient with HBsAg positive severe chronic aggressive hepatitis was dissociated into 5-6 fractions by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). The two of these fractions proved to be HBsAg and IgG and another three or four undetermined components. At the acute exacerbation period of this case, the fraction pattern of CIC by SDS-PAGE was similar to each other at any of the four stages and HBsAg always composed one of the antigens.