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Sequential changes in pancreatic markers in acute pancreatitis.
M Lempinen1, U H Stenman, P Puolakkainen
1Second Dept. of Surgery, Helsinki University Central Hospital, Helsinki, Finland.
Scandinavian Journal of Gastroenterology
|June 27, 2003
Summary
Trypsinogen-2 and its complex with alpha-1-antitrypsin (AAT) show more significant changes in acute pancreatitis (AP) than trypsinogen-1, suggesting a greater role in disease pathogenesis. Urinary pancreatic secretory trypsin inhibitor (PSTI) may indicate disease severity.
Area of Science:
- Gastroenterology
- Biochemistry
- Pathophysiology
Background:
- Acinar cell trypsinogen activation is key in acute pancreatitis (AP) pathogenesis.
- Characterizing temporal changes of trypsinogen-1, trypsinogen-2, their complexes with alpha-1-antitrypsin (AAT), trypsinogen activation peptide (TAP), and pancreatic secretory trypsin inhibitor (PSTI) is crucial for understanding AP.
Purpose of the Study:
- To characterize temporal changes of trypsinogen-1, trypsinogen-2, T1-AAT, T2-AAT, TAP, and PSTI in patients with AP.
- To investigate the role of these markers in AP pathogenesis and severity.
Main Methods:
- Serum and urine samples from 64 AP patients (19 severe) and 32 controls were analyzed.
- Time-resolved immunofluorometric assays (IFMA) measured trypsinogen-1, trypsinogen-2, PSTI, T1-AAT, and T2-AAT.
- Competitive enzyme immunoassay measured TAP.
Main Results:
- Urinary trypsinogen-2 excretion correlated strongly with AP severity, unlike trypsinogen-1.
- T2-AAT concentrations were higher in severe AP than mild AP, while T1-AAT showed no significant difference.
- Urinary PSTI correlated with AP severity, while plasma and urinary TAP decreased rapidly.
Conclusions:
- Trypsinogen-2 and its complex with AAT exhibit more pronounced changes in AP than trypsinogen-1, indicating a potentially larger role in pathogenesis.
- Urinary PSTI warrants further investigation as a potential marker for AP disease severity.