Related Experiment Video
Updated: Nov 7, 2025
Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Quantification of von Willebrand factor and ADAMTS-13 after traumatic injury: a pilot study
Taleen A MacArthur1, Julie Goswami1, Laurie Moon Tasson2
1Trauma, Critical Care and General Surgery, Mayo Clinic, Rochester, Minnesota, USA.
Background:
Von Willebrand factor (VWF) is an acute phase reactant synthesized in the megakaryocytes and endothelial cells. VWF forms ultra-large multimers (ULVWF) which are cleaved by the metalloprotease ADAMTS-13, preventing spontaneous VWF-platelet interaction. After trauma, ULVWF is released into circulation as part of the acute phase reaction. We hypothesized that trauma patients would have increased levels of VWF and decreased levels of ADAMTS-13 and that these patients would have accelerated thrombin generation.
Methods:
We assessed plasma concentrations of VWF antigen and ADAMTS-13 antigen, the Rapid Enzyme Assays for Autoimmune Diseases (REAADS) activity of VWF, which measure exposure of the platelet-binding A1 domain, and thrombin generation kinetics in 50 samples from 30 trauma patients and an additional 21 samples from volunteers. Samples were analyzed at 0 to 2 hours and at 6 hours from the time of injury. Data are presented as median (IQR) and Kruskal-Wallis test was performed between trauma patients and volunteers at both time points.
Results:
REAADS activity was greater in trauma patients than volunteers both at 0 to 2 hours (190.0 (132.0-264.0) vs. 92.0 (71.0-114.0), p<0.002) and at 6 hours (167.5 (108.0-312.5.0) vs. 92.0 (71.0-114.0), p<0.001). ADAMTS-13 antigen levels were also decreased in trauma patients both at 0 to 2 hours (0.84 (0.51-0.94) vs. 1.00 (0.89-1.09), p=0.010) and at 6 hours (0.653 (0.531-0.821) vs. 1.00 (0.89-1.09), p<0.001). Trauma patients had accelerated thrombin generation kinetics, with greater peak height and shorter time to peak than healthy volunteers at both time points.
Discussion:
Trauma patients have increased exposure of the VWF A1 domain and decreased levels of ADAMTS-13 compared with healthy volunteers. This suggests that the VWF burst after trauma may exceed the proteolytic capacity of ADAMTS-13, allowing circulating ULVWF multimers to bind platelets, potentially contributing to trauma-induced coagulopathy.
Level Of Evidence:
Prospective case cohort study.
Insights
Trauma patients show increased von Willebrand factor (VWF) activity and reduced ADAMTS-13 levels, leading to faster thrombin generation. This suggests a potential mechanism for trauma-induced coagulopathy.
Area of Science:
- Hematology
- Trauma Medicine
- Biochemistry
Background:
- Von Willebrand factor (VWF) is an acute phase reactant.
- VWF forms ultra-large multimers (ULVWF) cleaved by ADAMTS-13 to prevent platelet interaction.
- Trauma triggers an acute phase reaction, releasing ULVWF.
Purpose of the Study:
- To investigate VWF and ADAMTS-13 levels in trauma patients.
- To assess thrombin generation kinetics post-trauma.
- To determine the relationship between VWF, ADAMTS-13, and coagulopathy.
Main Methods:
- Prospective case cohort study.
- Assessed plasma VWF antigen, ADAMTS-13 antigen, and VWF REAADS activity.
- Measured thrombin generation kinetics in trauma patients and healthy volunteers.
Main Results:
- Trauma patients exhibited significantly higher VWF REAADS activity at 0-2 and 6 hours post-injury.
- ADAMTS-13 antigen levels were decreased in trauma patients at both time points.
- Trauma patients demonstrated accelerated thrombin generation kinetics.
Conclusions:
- Trauma patients show increased VWF A1 domain exposure and decreased ADAMTS-13.
- Elevated VWF post-trauma may overwhelm ADAMTS-13's capacity.
- This imbalance may contribute to trauma-induced coagulopathy.
