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Sodium Taurocholate Induced Severe Acute Pancreatitis in C57BL/6 Mice
Published on: June 28, 2021
Inflammatory mediators in human acute pancreatitis: clinical and pathophysiological implications
1Department of General Surgery, University Hospital of Ulm, Ulm, Germany.
Cytokine levels in acute pancreatitis (AP) correlate with organ dysfunction. An imbalance in interleukin-1 beta/interleukin-1 beta receptor antagonist (IL-1RA) indicates severe AP, while peak soluble IL-2 receptor (sIL-2R) predicts fatal outcomes.
Area of Science:
- Gastroenterology
- Immunology
- Critical Care Medicine
Background:
- The relationship between local/circulating cytokines, pancreatic inflammation, and organ dysfunction in acute pancreatitis (AP) remains unclear.
- Understanding these dynamics is crucial for managing AP complications.
Purpose of the Study:
- To investigate the time course and correlation of cytokine concentrations with pancreatic inflammation and organ dysfunction in AP.
- To identify specific cytokine profiles associated with disease severity and systemic complications.
Main Methods:
- Prospective clinical study involving 51 AP patients within 72 hours of symptom onset.
- Daily measurement of pro-inflammatory (IL-1β, IL-6, IL-8) and anti-inflammatory (IL-10, IL-1RA, sIL-2R) cytokines for seven days.
- Analysis of cytokine levels in ascites and lesser sac aspirates, correlated with organ complications.
Main Results:
- All measured cytokines were elevated in AP patients.
- Elevated sIL-2R, IL-10, and IL-6 were significantly associated with distant organ failure.
- An IL-1β/IL-1RA imbalance was observed in severe AP and pulmonary failure; peak sIL-2R predicted mortality.
- IL-6 emerged as the best prognostic marker for pulmonary failure.
Conclusions:
- Local mediator release, particularly an IL-1β/IL-1RA imbalance in severe cases, precedes systemic cytokine appearance.
- The observed patterns suggest systemic lymphocyte activation contributes to distant organ complications in severe AP.
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