Abstract
Aim
Hepatocytes biosynthesize about 80–90% of plasma complement proteins, including complement 3 (C3) and 4 (C4). The purpose of our study is to research the significance of complement in hepatitis B virus related cirrhosis (HBV-cirrhosis), discuss whether C3 and C4 could be served as available markers to assess liver function and prognostic in HBV-cirrhosis.
Methods
Blood samples were captured from 306 adult patients with HBV-cirrhosis, 23 chronic hepatitis B (CHB) without cirrhosis or liver failure, and 12 healthy adults. Serum C3 and C4 levels were compared in different groups, evaluating the correlation between C3/C4 levels and disease severity in patients with HBV-cirrhosis, analyzing the significance of complement components in infection and mortality of decompensated HBV-cirrhosis.
Results
The concentrations of C3 and C4 were markedly decreased in HBV-cirrhosis group than those in Chronic Hepatitis B (CHB) and healthy group (p < 0.05, respectively), especially in decompensated stage. In HBV-cirrhosis, The C3 and C4 levels were significantly negatively correlated with International Normalized Ratio (INR) and bilirubin, and significantly positively correlated with albumin, cholinesterase, cholesterol and platelet (p < 0.05, respectively). In addition, these were significance negative correlation with Child-Pugh score (C-P score), End-stage Liver Disease score (MELD score) and AST to platelet ratio (p < 0.05, respectively). More importantly, the C3 were significantly reduced in decompensated HBV-cirrhosis with infection or death, multivariate Cox-regression analysis revealed that lower C3 level was independent predictor of mortality in decompensated HBV-cirrhosis.
Conclusions
The C3 level could be served as available follow-up marker to evaluate liver function and disease severity in HBV-cirrhosis and superior to C4. Decreased C3 might be independent poor prognostic factor in patients with decompensated HBV-cirrhosis.
Longitudinal changes of liver function and hepatitis B reactivation in COVID‐19 patients with pre‐existing chronic hepatitis B virus infection