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1. Assessing Factor V Antigen and Degradation Products in Burn and Trauma Patients.

Author

Keyloun, John W, Le, Tuan D, Orfeo, Thomas, Brummel-Ziedins, Kathleen E, Bravo, Maria C, Kaye, Matthew D, Bourne, Dana E, Carney, Bonnie C, Freeman, Kalev, Mann, Kenneth G, Pusateri, Anthony E, Shupp, Jeffrey W, and SYSCOT Study Group

Subjects
SYSCOT Study Group, Humans, Blood Coagulation Disorders, Burns, Factor V, Factor Va, Injury Severity Score, Coagulopathy, Protein C, Trauma, Physical Injury - Accidents and Adverse Effects, Clinical Research, Clinical Sciences, Surgery
Abstract

IntroductionProposed mechanisms of acute traumatic coagulopathy (ATC) include decreased clotting potential due to factor consumption and proteolytic inactivation of factor V (FV) and activated factor V (FVa) by activated protein C (aPC). The role of FV/FVa depletion or inactivation in burn-induced coagulopathy is not well characterized. This study evaluates FV dynamics following burn and nonburn trauma.MethodsBurn and trauma patients were prospectively enrolled. Western blotting was performed on admission plasma to quantitate levels of FV antigen and to assess for aPC or other proteolytically derived FV/FVa degradation products. Statistical analysis was performed with Spearman's, Chi-square, Mann-Whitney U test, and logistic regression.ResultsBurn (n = 60) and trauma (n = 136) cohorts showed similar degrees of FV consumption with median FV levels of 76% versus 73% (P = 0.65) of normal, respectively. Percent total body surface area (TBSA) was not correlated with FV, nor were significant differences in median FV levels observed between low and high TBSA groups. The injury severity score (ISS) in trauma patients was inversely correlated with FV (ρ = -0.26; P = 0.01) and ISS ≥ 25 was associated with a lower FV antigen level (64% versus. 93%; P = 0.009). The proportion of samples showing proteolysis-derived FV was greater in trauma than burn patients (42% versus. 16%; P = 0.0006).ConclusionsIncreasing traumatic injury severity is associated with decreased FV antigen levels, and a greater proportion of trauma patient samples exhibit proteolytically degraded FV fragments. These associations are not present in burns, suggesting that mechanisms underlying FV depletion in burn and nonburn trauma are not identical.

Published
2022

2. Inhalation Injury is Associated with Endotheliopathy and Abnormal Fibrinolytic Phenotypes in Burn Patients: A Cohort Study

Author

Keyloun, John W, Le, Tuan D, Brummel-Ziedins, Kathleen E, Mclawhorn, Melissa M, Bravo, Maria C, Orfeo, Thomas, Johnson, Laura S, Moffatt, Lauren T, Pusateri, Anthony E, Shupp, Jeffrey W, McLawhorn, Melissa M, Callcut, Rachael A, Cohen, Mitchell J, Petzold, Linda R, Varner, Jeffrey D, Bravo, Maria Cristina, Freeman, Kalev, Mann, Kenneth G, Gautam, Aarti, Hammamieh, Rasha, and Jett, Marti

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Hematology, Physical Injury - Accidents and Adverse Effects, Clinical Research, Good Health and Well Being, Burns, Cohort Studies, Female, Humans, Male, Phenotype, Retrospective Studies, Thrombelastography, SYSCOT Study Group, Emergency & Critical Care Medicine, Clinical sciences, Allied health and rehabilitation science, Nursing
Abstract

Burn injury is associated with endothelial dysfunction and coagulopathy and concomitant inhalation injury (IHI) increases morbidity and mortality. The aim of this work is to identify associations between IHI, coagulation homeostasis, vascular endothelium, and clinical outcomes in burn patients. One hundred and twelve patients presenting to a regional burn center were included in this retrospective cohort study. Whole blood was collected at set intervals from admission through 24 hours and underwent viscoelastic assay with rapid thromboelastography (rTEG). Syndecan-1 (SDC-1) on admission was quantified by ELISA. Patients were grouped by the presence (n = 28) or absence (n = 84) of concomitant IHI and rTEG parameters, fibrinolytic phenotypes, SDC-1, and clinical outcomes were compared. Of the 112 thermally injured patients, 28 (25%) had IHI. Most patients were male (68.8%) with a median age of 40 (interquartile range, 29-57) years. Patients with IHI had higher overall mortality (42.68% vs 8.3%; P < .0001). rTEG LY30 was lower in patients with IHI at hours 4 and 12 (P < .05). There was a pattern of increased abnormal fibrinolytic phenotypes among IHI patients. There was a greater proportion of IHI patients with endotheliopathy (SDC-1 > 34 ng/ml) (64.7% vs 26.4%; P = .008). There was a pattern of increased mortality among patients with IHI and endotheliopathy (0% vs 72.7%; P = .004). Significant differences between patients with and without IHI were found in measures assessing fibrinolytic potential and endotheliopathy. Mortality was associated with abnormal fibrinolysis, endotheliopathy, and IHI. However, the extent to which IHI-associated dysfunction is independent of TBSA burn size remains to be elucidated.

Published
2022

7. TACTIC: Trans‐Agency Consortium for Trauma‐Induced Coagulopathy

Author

Mann, K.G., Freeman, K., Mann, Kenneth G., Esmon, Charles T., Wisnewski, Stephen, Tracy, Russell P., Kindzelski, Andrei L., Pusateri, Anthony, Banerjee, Anirban, Brass, Lawrence F., Brummel‐Ziedins, Kathleen E., Butenas, Saulius, Cohen, Mitchell J., Diamond, Scott L., Freeman, Kalev, Moore, Ernest E., Morrissey, James H., Nelson, Mark T., Park, Myung S., Ruf, Wolfram, Shupp, Jeffrey W., Sperry, Jason L., Spiess, Bruce D., Stalker, Timothy J., and Zuckerbraun, Brian S.

Published
2015
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11. Factor Xa Inhibition Reduces Coagulation Activity but Not Inflammation Among People With HIV: A Randomized Clinical Trial

Author

Baker, Jason V, primary, Wolfson, Julian, additional, Peterson, Tess, additional, Mooberry, Micah, additional, Gissel, Matthew, additional, Mystakelis, Harry, additional, Henderson, Michael W, additional, Garcia-Myers, Kelly, additional, Rhame, Frank S, additional, Schacker, Timothy W, additional, Brummel-Ziedins, Kathleen E, additional, Sereti, Irini, additional, Key, Nigel S, additional, and Tracy, Russell P, additional

Published
2020
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14. FcγRIIa

Author

Schneider, David J., primary, McMahon, Sean R., additional, Chava, Sreedivya, additional, Taatjes-Sommer, Heidi S., additional, Meagher, Sean, additional, Ehle, Gregory L., additional, and Brummel-Ziedins, Kathleen E., additional

Published
2018
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20. Reference ranges for rotational thromboelastometry in male Sprague Dawley rats.

Author

Vigiola Cruz, Mariana, Luker, Jenna N., Carney, Bonnie C., Brummel-Ziedins, Kathleen E., Bravo, Maria-Cristina, Orfeo, Thomas, Chen, Jason H., Moffatt, Lauren T., and Shupp, Jeffrey W.

Subjects
ANIMAL experimentation, BLOOD coagulation, BLOOD coagulation disorders, BLOOD coagulation tests, RATS, REFERENCE values, THROMBELASTOGRAPHY, LABORATORY equipment & supplies
Abstract

Background: A functional coagulation assay was used to investigate the extrinsic pathway of coagulation on citrated whole blood samples from healthy adult male Sprague Dawley rats using the mini cup and pin system. Methods: Reference values for coagulation parameters from forty-three animals were calculated using data obtained from the ROTEM® delta hemostasis analyzer with the EXTEM test. Results: The following ranges, presented as the 2.5-97.5 percentiles, were established: CT [18-77], CFT [20-80], α [73-86], MCF [53-70], and ML [1-22], along with others. Conclusions: These reference ranges can be used in future studies in rats to identify clinically significant coagulopathies. [ABSTRACT FROM AUTHOR]

Published
2017
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21. The influence of prophylactic factor VIII in severe hemophilia A

Author

Gissel, Matthew, Whelihan, Matthew F, Ferris, Lauren A, Mann, Kenneth G, Rivard, Georges E, and Brummel-Ziedins, Kathleen E

Subjects
Adult, Cohort Studies, Young Adult, Factor VIII, Adolescent, Blotting, Western, Thrombin, Humans, Regression Analysis, Computer Simulation, Hemophilia A, Blood Coagulation, Article
Abstract

Haemophilia A individuals displaying a similar genetic defect have heterogeneous clinical phenotypes. Our objective was to evaluate the underlying effect of exogenous factor (f)VIII on tissue factor (Tf)-initiated blood coagulation in severe haemophilia utilizing both empirical and computational models. We investigated twenty-five clinically severe haemophilia A patients. All individuals were on fVIII prophylaxis and had not received fVIII from 0.25 to 4 days prior to phlebotomy. Coagulation was initiated by the addition of Tf to contact-pathway inhibited whole blood ± an anti-fVIII antibody. Aliquots were quenched over 20 min and analyzed for thrombin generation and fibrin formation. Coagulation factor levels were obtained and used to computationally predict thrombin generation with fVIII set to either zero or its value at the time of the draw. As a result of prophylactic fVIII, at the time of the blood draw, the individuals had fVIII levels that ranged from1% to 22%. Thrombin generation (maximum level and rate) in both empirical and computational systems increased as the level of fVIII increased. FXIII activation rates also increased as the fVIII level increased. Upon suppression of fVIII, thrombin generation became comparable in both systems. Plasma composition analysis showed a negative correlation between bleeding history and computational thrombin generation in the absence of fVIII. Residual prophylactic fVIII directly causes an increase in thrombin generation and fibrin cross-linking in individuals with clinically severe haemophilia A. The combination of each individual's coagulation factors (outside of fVIII) determine each individual's baseline thrombin potential and may affect bleeding risk.

Published
2011

23. From Principle to Practice: Bridging the Gap in Patient Profiling

Author

Foley, Jonathan H., primary, Orfeo, Thomas, additional, Undas, Anetta, additional, McLean, Kelley C., additional, Bernstein, Ira M., additional, Rivard, Georges-Etienne, additional, Mann, Kenneth G., additional, Everse, Stephen J., additional, and Brummel-Ziedins, Kathleen E., additional

Published
2013
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40. Antithrombotic properties of aspirin and resistance to aspirin: beyond strictly antiplatelet actions

Author

Undas, Anetta, Brummel-Ziedins, Kathleen E., and Mann, Kenneth G.

Abstract

Aspirin is effective in the prevention of cardiovascular events in high-risk patients. The primary established effect of aspirin on hemostasis is to impair platelet aggregation via inhibition of platelet thromboxane A2 synthesis, thus reducing thrombus formation on the surface of the damaged arterial wall. Growing evidence also indicates that aspirin exerts additional antithrombotic effects, which appear to some extent unrelated to platelet thromboxane A2 production. Aspirin can reduce thrombin generation with the subsequent attenuation of thrombin-mediated coagulant reactions such as factor XIII activation. Aspirin also acetylates lysine residues in fibrinogen resulting in increased fibrin clot permeability and enhanced clot lysis as well as directly promoting fibrinolysis with high-dose aspirin. The variable effectiveness of aspirin in terms of clinical outcomes and laboratory findings, which has been termed aspirin resistance, may be related to these additional antithrombotic effects that are altered when associated with common genetic polymorphisms such as the Leu33Pro β3-integrin or Val34Leu factor XIII mutations. However, the clinical relevance of these observations is still unclear. Elucidation of the actual impacts of aspirin other than antiaggregation effects could be important in view of the widespread use of this drug in the prevention of thrombotic manifestations of atherosclerosis.

Published
2007
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