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Updated: May 6, 2026

Sodium Taurocholate Induced Severe Acute Pancreatitis in C57BL/6 Mice
Published on: June 28, 2021
Endotoxaemia and complement activation in acute pancreatitis in man
Endotoxemia and complement activation are linked to severe acute pancreatitis. Increased C3 catabolism and endotoxemia correlate with systemic complications and fatal outcomes in pancreatitis patients.
Area of Science:
- Biochemistry
- Immunology
- Gastroenterology
Background:
- Acute pancreatitis is a serious condition with potential systemic complications.
- Endotoxemia, the presence of bacterial endotoxins in the bloodstream, may play a role in pancreatitis severity.
- Complement system activation is implicated in inflammatory diseases.
Purpose of the Study:
- To investigate the presence and significance of endotoxemia in acute pancreatitis.
- To assess the relationship between endotoxemia, complement activation (C3 catabolism), and clinical outcomes in pancreatitis patients.
Main Methods:
- Studied 24 patients with 26 acute pancreatitis attacks.
- Measured endotoxemia using the limulus lysate assay.
- Assessed C3 catabolism and complement activation levels.
Main Results:
- Endotoxemia was detected in 13 of 26 pancreatitis attacks.
- Six of seven patients with systemic complications had endotoxemia.
- C3 catabolism was elevated in all attacks; falling C3 levels correlated with fatal outcomes.
- Increased complement activation was observed in patients with detected endotoxemia.
Conclusions:
- Endotoxemia is frequently present in acute pancreatitis and associated with systemic complications.
- Complement activation, indicated by C3 catabolism, is a consistent finding in pancreatitis and a marker of severity.
- These findings suggest endotoxemia and complement activation are critical factors in acute pancreatitis pathogenesis and prognosis.
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