Evaluation of N-terminal propeptide of procollagen type III for Live fibrosis

Abstract

Background: Hepatic stellate cells promote fibrosis, responding to injury and inflammation, causing excessive accumulation of ECM and liver fibrosis. The N-terminal peptide of type III procollagen (PIIINP) is released during the synthesis of type III collagen and is a direct indicator of ECM collagen accumulation. Excessive accumulation of ECM in the space of Disse is the main characteristic of liver fibrosis5,6. Aim: To evaluate the effect of clinical severity of liver fibrosis on the serum level of PIIINP. Materials and Methods: We used a cross-sectional study design. We included 42 patients who were admitted to Third State Central Hospital from February 2024 to July 2024 and fulfilled the study’s criteria. We collected serum samples to measure PIIINP levels using an ELISA kit, and percutaneous liver biopsies were obtained for histopathology. The study was approved and carried out by the 23/001 protocol of the Ethical Committee. STATA-14 was used for analysis, and correlation and mean differences were calculated using ANOVA. Results: The study patients were females n=31 (26.2%) and males n=11 (26.2%). A Metavir scoring system was used to classify liver fibrosis grades. We divided into 3 groups: minimal or no fibrosis (F0-1), advanced fibrosis (F2-3), and Liver cirrhosis (F4). A moderate positive correlation was found between PIIINP level and liver fibrosis grade (p=0.03). There was a significant statistical difference in serum mean PIIINP level between the F0-1 and F2-3 groups (p=0.05). The accuracy of the test, according to AUC, was 0.714. When we set the PIIINP cut-off value to ≥15.15ng/ml, sensitivity and specificity were 71.4% and 74.3%, respectively. Conclusion: Our study concluded that serum PIIINP level is a direct biomarker of liver fibrosis and cirrhosis.