Frontiers in immunology · 2026
Evaluation of oxidative stress in acute pancreatitis.
СтатьяНаблюдательное исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Pădureanu Vlad, Florescu Dan Nicolae, Cazacu Sergiu Marian, Rădulescu Virginia Maria, Pădureanu Rodica, Podeanu Mihaela Andreea, Mititelu Radu Razvan, Pomacu Mihnea Marian, Bugă Ana Maria
Аннотация
BACKGROUND: Oxidative stress is implicated in acute pancreatitis (AP), but its diagnos-tic/prognostic value at presentation is uncertain; this study evaluated whether redox markers discriminate radiologic severity and how they relate to inflammation and apoptosis.
METHODS: In this observational study cohort severity was classified as Balthazar D vs A-C score. Assays biomarkers included protein carbonyls (P-carb), lipid peroxidation state (TBARS), antioxidant status (TAC), reduced glutathione (GSH), catalase (CAT); inflammatory markers (CRP, AISI, SIRI); pro-apoptosis/innate immunity markers (caspase-3, IL-1β, AIM2). Discrimination used ROC/AUC with bootstrap CIs; a prespecified Redox Imbalance Index (RII) and exploratory load-vs-buffer ratios were derived. Correlations employed Spearman and age-adjusted partial Spearman with Benjamini Hochberg-FDR correction; logistic models used z-scored predictors with.632 bootstrap correction.
RESULTS: Single-marker discrimination was modest (GSH AUC of 0.57 [95% CI 0.24-0.85]; CRP of 0.55 [0.26-0.82]; AISI of 0.53 [0.30-0.75]); RII of 0.42 [0.17-0.69]; derived indices (POBI ≤ 0.48). Combined models overfit (apparent AUC 0.56-0.59;.632 corrected ≈0.39). By contrast, caspase-3 correlated with CRP, GSH, and P-carb (moderate, age-robust), and GSH-P-carb coupling was strong, whereas TBARS aligned weakly.
CONCLUSIONS: At presentation, oxidative-stress signatures co-vary with inflammation and apoptosis (strong GSH-P-carb coupling and moderate, age-robust caspase-3 correlations with CRP and P-carb). However, neither single markers nor composite indices (including the prespecified Redox Imbalance Index) reliably discriminated radiologic severity (AUCs 0.42-0.57, all 95% CIs including 0.50). Multivariable models showed substantial overfitting after.632 bootstrap correction. These findings support further investigation of the antioxidant-protein-oxidation and apoptosis-inflammation axes in adequately powered, longitudinal studies rather than as immediate clinical triage tools.
METHODS: In this observational study cohort severity was classified as Balthazar D vs A-C score. Assays biomarkers included protein carbonyls (P-carb), lipid peroxidation state (TBARS), antioxidant status (TAC), reduced glutathione (GSH), catalase (CAT); inflammatory markers (CRP, AISI, SIRI); pro-apoptosis/innate immunity markers (caspase-3, IL-1β, AIM2). Discrimination used ROC/AUC with bootstrap CIs; a prespecified Redox Imbalance Index (RII) and exploratory load-vs-buffer ratios were derived. Correlations employed Spearman and age-adjusted partial Spearman with Benjamini Hochberg-FDR correction; logistic models used z-scored predictors with.632 bootstrap correction.
RESULTS: Single-marker discrimination was modest (GSH AUC of 0.57 [95% CI 0.24-0.85]; CRP of 0.55 [0.26-0.82]; AISI of 0.53 [0.30-0.75]); RII of 0.42 [0.17-0.69]; derived indices (POBI ≤ 0.48). Combined models overfit (apparent AUC 0.56-0.59;.632 corrected ≈0.39). By contrast, caspase-3 correlated with CRP, GSH, and P-carb (moderate, age-robust), and GSH-P-carb coupling was strong, whereas TBARS aligned weakly.
CONCLUSIONS: At presentation, oxidative-stress signatures co-vary with inflammation and apoptosis (strong GSH-P-carb coupling and moderate, age-robust caspase-3 correlations with CRP and P-carb). However, neither single markers nor composite indices (including the prespecified Redox Imbalance Index) reliably discriminated radiologic severity (AUCs 0.42-0.57, all 95% CIs including 0.50). Multivariable models showed substantial overfitting after.632 bootstrap correction. These findings support further investigation of the antioxidant-protein-oxidation and apoptosis-inflammation axes in adequately powered, longitudinal studies rather than as immediate clinical triage tools.