Comparative evaluation of Hepassocin, DCP, and AFP-L3 for non-invasive assessment of liver fibrosis in Hepatitis B infection

Hepatitis B virus (HBV) infection often leads to progressive liver fibrosis, which may remain undetected until irreversible hepatic damage occurs. This study evaluated Hepassocin (HPS), des-gamma-carboxy Prothrombin (DCP) and Lens culinaris agglutinin-reactive fraction of alpha-fetoprotein (AFP-L3) as serological indicators associated with APRI-defined fibrosis risk in HBV infection. This observational study included 150 HBsAg-positive patients (acute and chronic HBV) and 50 healthy controls. Serum concentrations of HPS, DCP and AFP-L3 were quantified using ELISA alongside routine liver function tests. Fibrosis risk was evaluated with the AST-to-Platelet Ratio Index (APRI) and classified based on recognized clinical cut-offs. Group comparisons using non-parametric testing, correlations were assessed by Spearman correlation and binary logistic regression was applied to identify independent predictors of severe fibrosis. Diagnostic accuracy was assessed using ROC analysis. HBV patients exhibited significantly altered liver biochemistry, including elevated liver enzymes, reduced platelet counts, higher APRI scores, and increased serum levels of all three biomarkers compared with controls. HPS and DCP levels increased progressively across APRI-defined fibrosis categories, whereas AFP-L3 showed limited discriminatory ability. Multivariate analysis identified HPS and DCP as biomarkers independently associated with higher APRI-defined fibrosis risk, while AFP-L3 lacked independent predictive value. ROC analysis showed that HPS and DCP demonstrated good discrimination for higher APRI-defined fibrosis risk categories within the study population, and their combined use further improved diagnostic performance. The integrated HPS + DCP model demonstrated the highest discriminatory performance within APRI-based fibrosis risk stratification (AUC = 0.935). HPS and DCP are potential non-invasive biomarkers associated with APRI-defined fibrosis risk in HBV infection and showed superior predictive performance compared with AFP-L3 and routine biochemical markers within APRI-based fibrosis stratification. Their combined application may enhance APRI-based fibrosis risk stratification; however, these findings should be considered preliminary and require validation in independent cohorts using accepted fibrosis reference standards before clinical adoption can be considered.