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Complement Component 3 as a Surrogate Hallmark for Metabolic Abnormalities in Patients with Chronic Hepatitis C
Takashi Himoto1, Eiichiro Hirakawa1, Koji Fujita2
1Department of Medical Technology, Kagawa Prefectural University of Health Sciences, Kagawa, Japan.
Annals of Clinical and Laboratory Science
|March 1, 2019
Summary
Elevated serum complement component 3 (C3) levels in chronic hepatitis C patients correlate with obesity and insulin resistance. Increased C3 may indicate hepatic steatosis and fibrosis, but not necessarily hepatocyte C3 expression.
Area of Science:
- Hepatology
- Immunology
- Metabolic Syndrome
Background:
- Chronic hepatitis C (CH-C) is associated with metabolic abnormalities.
- Complement component 3 (C3) plays a role in immune responses and inflammation.
- The relationship between C3 and metabolic/histological changes in CH-C is not fully understood.
Purpose of the Study:
- To investigate the correlation between serum C3 levels and metabolic abnormalities (obesity, insulin resistance) in CH-C patients.
- To examine the association between serum C3 levels and histological features (hepatic steatosis, fibrosis) in CH-C.
- To evaluate the degree of hepatic C3 expression and its relation to serum C3 levels.
Main Methods:
- Serum C3 levels were measured.
- Obesity assessed by body mass index (BMI).
- Insulin resistance estimated using homeostasis model for assessment of insulin resistance (HOMA-IR).
- Hepatic steatosis and fibrosis evaluated using established classification systems.
- Hepatic C3 expression examined via immunohistochemistry.
Main Results:
- Serum C3 levels significantly correlated with BMI, HOMA-IR, and serum triglyceride levels.
- Serum C3 levels increased proportionally with the severity of hepatic steatosis.
- Serum C3 levels showed a trend of increase with advancing hepatic fibrosis.
- Hepatic C3 expression in hepatocytes was not associated with serum C3 levels.
Conclusions:
- Elevated serum C3 levels in CH-C patients may reflect underlying obesity, insulin resistance, and/or hepatic steatosis.
- Increased C3 synthesis in CH-C might originate from non-hepatocyte cells.
- Further research is needed to elucidate the precise role of C3 in CH-C pathogenesis.
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