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Evaluate TAP and trypsin-2 as biomarkers for predicting systemic inflammation in acute pancreatitis.

January 6, 2026Medicina0 citationsOpen Access

Integrating Bayesian Inference and Machine Learning to Evaluate TAP and Trypsin-2 as Early Biomarkers of Systemic Inflammation in Acute Pancreatitis

AFAlina Calin FrijGrigore T. Popa University of Medicine and Pharmacy CVCristian VelicescuGrigore T. Popa University of Medicine and Pharmacy AAAndrei AndoneGrigore T. Popa University of Medicine and Pharmacy

Key Points

Evaluate TAP and trypsin-2 as biomarkers for predicting systemic inflammation in acute pancreatitis.
Retrospective cohort analysis of 54 acute pancreatitis patients
Evaluated serum and urinary markers using Bayesian correlation and machine learning
Analyzed relationships with inflammation and enzymatic activities
Bayesian analysis revealed relationships between serum TAP and CRP levels
Mediation analysis found TAP and trypsin-2 accounted for 42–44% of CRP's impact on enzyme elevation
Random Forest model identified urinary trypsin-2 as a significant predictor of inflammation

Abstract

Background and Objectives: Acute pancreatitis (AP) has a wide range of clinical severity, and early prediction of disease progression is still challenging. Trypsinogen-activating peptide (TAP) and trypsin-2 serve as direct biomarkers for intrapancreatic proteolytic activation and may provide earlier pathophysiological information compared with traditional markers. Materials and Methods: In this retrospective cohort analysis involving 54 AP patients, we evaluated 24 h serum and urinary TAP and trypsin-2 concentrations by Bayesian correlation, mediation analysis, unsupervised K-means clustering, and supervised machine learning (Elastic Net and Random Forest). The analyses investigated the relationships of biomarkers with inflammation (CRP), enzymatic activities (amylase, lipase), and clinical factors, as well as inflammation severity (CRP levels). Results: Bayesian correlations indicated moderate evidence for a relationship between serum TAP and CRP (BF10 = 8.42), as well as strong evidence linking age to serum TAP (BF10 = 12.75). Serum trypsin-2 showed no correlation with CRP, while urinary trypsin-2 had a correlation with amylase (BF10 = 6.89). Mediation analysis indicated that TAP and trypsin-2 accounted for 42–44% of the impact of CRP on pancreatic enzyme elevation. Clustering revealed three phenotypic subgroups (“Mild Activation”, “Moderate System”, and “Severe Pancreatic-Renal”), the latter showing the highest levels of CRP and biomarkers. Machine learning models highlighted urinary trypsin-2 and age as the most significant predictors of inflammation, with Random Forest achieving the highest performance (R2 = 0.53). Conclusions: Early urinary trypsin-2 outperforms serum markers as a predictor of systemic inflammatory intensity, indicating total proteolytic impairment and renal clearance. This integrative analysis reveals unique biological phenotypes and highlights the potential of these biomarkers for early assessment of the inflammatory burden. Their role in predicting clinical disease progression requires prospective validation. Integrative biomarker analysis reveals unique biological phenotypes and improves assessment of inflammatory burden in PA. Larger cohorts are required for prospective validation to incorporate these biomarkers into precision-based diagnostic frameworks.

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