Literature DB >> 30086072

The procoagulant molecule plasminogen activator inhibitor-1 is associated with injury severity and shock in patients with and without traumatic brain injury.

Mary Condron1, Susan Rowell, Elizabeth Dewey, Taylor Anderson, Lelani Lealiiee, David Farrell, Holly Hinson.   

Abstract

BACKGROUND: Traumatic injury is associated with an increased risk of coagulopathy and venous thrombosis. plasminogen activator inhibitor-1 (PAI-1) is a procoagulant molecule that inhibits tPA/uPA, thrombomodulin, and activated protein C. We hypothesized that elevated PAI-1 levels would be associated with increased Injury Severity Score (ISS) in injured patients with and without traumatic brain injury and that PAI-1 levels would vary with injury type.
METHODS: We retrospectively analyzed demographic, ISS, and hemodynamic data from a prospectively collected database. Patients with traumatic injury requiring intensive care unit admission (n = 268) were classified as multiple injuries, isolated body, or isolated head based on Abbreviated Injury Severity score. Admission PAI-1 levels were quantified using a Luminex analyte platform. Univariate tests for association informed the construction of a multivariate model of the relationship between PAI-1 and ISS.
RESULTS: Plasminogen activator inhibitor-1 positively associated with ISS (p < 0.0001) and was highest in patients with ISS greater than 35 (p < 0.0001). Plasminogen activator inhibitor-1 was significantly different between multiple injuries, isolated body, and isolated head patients (p < 0.0001). On univariate analysis, age (p = 0.0011), hypotension (p = 0.0076), and alcohol intoxication (p = 0.0024) were all positively associated with PAI-1 level. Admission international normalized ratio was not associated with PAI-1 level (p = 0.638). After adjusting for age, sex, hypotension, and alcohol intoxication, higher PAI-1 levels were associated with higher ISS (p < 0.0001).
CONCLUSION: Elevated PAI-1 at admission is associated with higher ISS. This association is more pronounced in patients with hypotension. These findings suggest that PAI-1 levels may reflect the burden of endothelial damage and platelet activation after injury. LEVEL OF EVIDENCE: Prognostic, level III.

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Year:  2018        PMID: 30086072      PMCID: PMC6309418          DOI: 10.1097/TA.0000000000002040

Source DB:  PubMed          Journal:  J Trauma Acute Care Surg        ISSN: 2163-0755            Impact factor:   3.313


  22 in total

1.  The International Normalized Ratio overestimates coagulopathy in stable trauma and surgical patients.

Authors:  Sean P McCully; Loic J Fabricant; Nicholas R Kunio; Tahnee L Groat; Katherine M Watson; Jerome A Differding; Thomas G Deloughery; Martin A Schreiber
Journal:  J Trauma Acute Care Surg       Date:  2013-12       Impact factor: 3.313

Review 2.  PAI-1, progress in understanding the clinical problem and its aetiology.

Authors:  Takayuki Iwaki; Tetsumei Urano; Kazuo Umemura
Journal:  Br J Haematol       Date:  2012-02-24       Impact factor: 6.998

3.  Elevation of plasma free PAI-1 levels as an integrated endothelial response to severe burns.

Authors:  K Aoki; N Aikawa; K Sekine; M Yamazaki; T Mimura; T Urano; A Takada
Journal:  Burns       Date:  2001-09       Impact factor: 2.744

4.  Among inflammation and coagulation markers, PAI-1 is a true component of the metabolic syndrome.

Authors:  I Mertens; A Verrijken; J J Michiels; M Van der Planken; J B Ruige; L F Van Gaal
Journal:  Int J Obes (Lond)       Date:  2006-01-03       Impact factor: 5.095

Review 5.  Plasminogen activator inhibitor (PAI)-1 in vascular inflammation and thrombosis.

Authors:  Yoshimasa Aso
Journal:  Front Biosci       Date:  2007-05-01

6.  Early coagulopathy after traumatic brain injury: the role of hypoperfusion and the protein C pathway.

Authors:  Mitchell Jay Cohen; Karim Brohi; Michael T Ganter; Geoffrey T Manley; Robert C Mackersie; Jean-François Pittet
Journal:  J Trauma       Date:  2007-12

7.  Trauma-induced coagulopathy: standard coagulation tests, biomarkers of coagulopathy, and endothelial damage in patients with traumatic brain injury.

Authors:  Gustav Folmer Genét; Pär Ingemar Johansson; Martin Abild Stengaard Meyer; Sacha Sølbeck; Anne Marie Sørensen; Claus Falck Larsen; Karen Lise Welling; Nis Agerlin Windeløv; Lars S Rasmussen; Sisse Rye Ostrowski
Journal:  J Neurotrauma       Date:  2013-02-05       Impact factor: 5.269

8.  Epidemiology of trauma deaths: a reassessment.

Authors:  A Sauaia; F A Moore; E E Moore; K S Moser; R Brennan; R A Read; P T Pons
Journal:  J Trauma       Date:  1995-02

9.  Overwhelming tPA release, not PAI-1 degradation, is responsible for hyperfibrinolysis in severely injured trauma patients.

Authors:  Michael P Chapman; Ernest E Moore; Hunter B Moore; Eduardo Gonzalez; Fabia Gamboni; James G Chandler; Sanchayita Mitra; Arsen Ghasabyan; Theresa L Chin; Angela Sauaia; Anirban Banerjee; Christopher C Silliman
Journal:  J Trauma Acute Care Surg       Date:  2016-01       Impact factor: 3.313

10.  Deep vein thrombosis prophylaxis in trauma patients.

Authors:  Serdar Toker; David J Hak; Steven J Morgan
Journal:  Thrombosis       Date:  2011-05-15
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