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Sodium Taurocholate Induced Severe Acute Pancreatitis in C57BL/6 Mice
Published on: June 28, 2021
Acute pancreatitis induces a transient hypercoagulable state in murine models
Pavan Rao1, Britney Niemann2, Brett Szeligo3
1Department of Surgery, Allegheny Health System, Pittsburgh, PA, USA; Division of Surgical Oncology, Department of Surgery, West Virginia University, Morgantown, WV, USA.
Acute pancreatitis (AP) causes a temporary hypercoagulable state, increasing venous thromboembolism (VTE) risk. Thromboelastography (TEG) can assess this AP-induced hypercoagulability in both mice and humans.
Area of Science:
- Coagulation science
- Pancreatology
- Thrombosis research
Background:
- Venous thromboembolism (VTE) risk is elevated in acute pancreatitis (AP), though not well-studied.
- Hypercoagulable states contribute to VTE, but their role in AP requires further elucidation.
Purpose of the Study:
- To characterize the hypercoagulable state in AP using thromboelastography (TEG).
- To assess the utility of TEG as a point-of-care test for AP-related coagulation changes.
Main Methods:
- AP was induced in mice using L-arginine and caerulein; TEG was performed on native samples.
- Platelet aggregation, circulating tissue factor (TF), and VTE in a murine model were assessed.
- Human AP patient blood samples were analyzed using TEG.
Main Results:
- Mice with AP showed increased maximum amplitude (MA) and coagulation index (CI) via TEG, indicating hypercoagulability.
- Hypercoagulability peaked at 24 hours post-induction and normalized by 72 hours.
- Increased platelet aggregation, elevated TF, and enhanced clot formation were observed in AP models.
- Over two-thirds of human AP patients exhibited elevated MA and CI, confirming hypercoagulability.
Conclusions:
- AP induces a transient hypercoagulable state in mice, detectable by TEG.
- Correlative evidence suggests hypercoagulability in human AP.
- Further research is needed to link TEG-derived coagulation measures to VTE incidence in AP.
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