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Kinin activation and protease inhibitors in acute pancreatitis in man
Abstract:
The changes in the protease inhibitors and in the kallikrein-kinin system were analysed in 19 attacks of acute pancreatitis in man and correlated to the severity and clinical course of the disease. Functional alpha 2-macroglobulin was 5% in peritoneal fluid and 32% in blood in severe attacks. Functional Cl inactivator was zero in the peritoneal fluid, while values were normal in blood. High levels of complexes between alpha 1-proteinase inhibitor and trypsin were found during the first 6 days of illness in severe attacks, especially in the peritoneal fluid. Prekallikrein, kininogen and kallikrein inhibition were significantly lower in blood in severe attacks than in moderate or mild attacks. These changes were even more pronounced in the peritoneal fluid, where kallikrein-like activity was above normal, while kininogen and kallikrein inhibition were zero in severe attacks. Both high and low molecular weight kininogen were decreased, denoting an activation also by kininogenases other than plasma kallikrein. In conclusion, kinin activation was demonstrated in acute pancreatitis, especially in the peritoneal fluid. Kinin activation and protease inhibitory activity were closely correlated to the severity and clinical course of the disease. Tryptic activation of the kinin system seems probable at the low alpha 2-macroglobulin levels found in severe attacks, according to our earlier in vitro studies.
Insights
Kinin activation and protease inhibitor changes correlate with acute pancreatitis severity. Severe attacks show reduced inhibitors and increased kinin activity, particularly in peritoneal fluid, suggesting tryptic activation.
Area of Science:
- Biochemistry
- Physiology
- Pathology
Background:
- Acute pancreatitis involves complex protease and kinin system dysregulation.
- Understanding these changes is crucial for assessing disease severity and clinical course.
Purpose of the Study:
- To analyze protease inhibitor and kallikrein-kinin system alterations in acute pancreatitis.
- To correlate these changes with disease severity and clinical outcomes.
Main Methods:
- Analysis of protease inhibitors (alpha 2-macroglobulin, Cl inactivator, alpha 1-proteinase inhibitor) and kallikrein-kinin system components (prekallikrein, kininogen, kallikrein activity/inhibition).
- Correlation of measured parameters with disease severity and clinical course in 19 human acute pancreatitis attacks.
- Comparison of levels in blood and peritoneal fluid.
Main Results:
- Severe attacks showed significantly reduced functional alpha 2-macroglobulin and Cl inactivator in peritoneal fluid.
- High levels of alpha 1-proteinase inhibitor-trypsin complexes were observed in severe attacks.
- Decreased prekallikrein, kininogen, and kallikrein inhibition were noted in blood and peritoneal fluid during severe pancreatitis, with increased kallikrein-like activity in peritoneal fluid.
Conclusions:
- Kinin activation occurs in acute pancreatitis, predominantly in the peritoneal fluid.
- Protease inhibitory activity and kinin activation are closely linked to disease severity and clinical course.
- Tryptic activation of the kinin system is suggested in severe pancreatitis due to low alpha 2-macroglobulin levels.
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