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1 Department of Pediatrics, University of Alabama at Birmingham, Birmingham, AL, USA
2 Division of Allergy, Pulmonary and Critical Care Medicine, Vanderbilt University, Nashville, TN, USA
3 Division of Pulmonary and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, AL, USA
4 Cardiovascular Research Institute, University of California at San Francisco, San Francisco, CA, USA
5 Division of Pulmonary and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, AL, USA; Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA
* To whom correspondence should be addressed. E-mail: olman{at}uab.edu.
The alveolar fibrinolytic system is altered in acute lung injury. Levels of the fibrinolytic protease inhibitor, plasminogen activator inhibitor-1 (PAI-1), are too low in bronchoalveolar lavage to address its prognostic significance. This study was performed to assess whether PAI-1 antigen antigen in undiluted pulmonary edema fluid can identify patients with acute lung injury and predict their outcome. PAI-1 antigen levels in both plasma and edema fluid were higher in acute lung injury compared with hydrostatic edema, and edema fluid PAI-1 values identified those with acute lung injury with high sensitivity and specificity. Both the high plasma and edema fluid PAI-1 antigen values were associated with a higher motality rate and fewer days of unassisted ventilation in patients with acute lung injury. Differences in PAI-1 activity were concordant with levels of PAI-1 antigen. While the fibrin-derived alveolar D dimer levels were strikingly similar in both groups, acute lung injury patients had a higher relative proportion of D monomer. In conclusion, PAI-1 levels in edema fluid and plasma identify those with acute lung injury that have a poor prognosis. The data indicate that fibrin turnover in early acute lung injury is a consequence of a rapid fibrinogen influx and fractional fibrinolytic inhibition.
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