Diagnostic Accuracy of Pleural Fluid Polymorphonuclear Elastase in the Differentiation between Pyogenic Bacterial Infectious and Non-Infectious Pleural Effusions

Abstract

Background and Objectives: To establish the diagnostic accuracy of the markers of neutrophil activity (elastase and lysozyme) determined in pleural fluid, for differentiating between pyogenic bacterial infectious and non-infectious pleural effusions. Patients and Methods: At our tertiary referral teaching hospital, 160 patients over 14 years with pleural effusion (PE), classified as pyogenic bacterial infectious (41 parapneumonic complicated, 32 parapneumonic non-complicated) and non-infectious (32 neoplasm and 55 undiagnosed pleural exudates) were examined in a prospective study. Polymorphonuclear elastase (PMN-E) was determined by an immunoactivation method and lysozyme by a turbidimetric method. Receiver operating characteristic (ROC) curves were used to evaluate diagnostic accuracy. Results: Pleural fluid PMN-E was the biochemical marker that best differentiated between pyogenic bacterial infectious and non-infectious PE. The ROC area under the curve (AUC) for PMN-E was 0.8276. A PMN-E value over 230 µg/l diagnosed infectious PE with a specificity of 0.81 and a sensitivity of 0.74. The ROC AUC for proteins plus lactate dehydrogenase was 0.7430. Differences between the two ROC curves were significant (p = 0.032). After excluding purulent parapneumonic complicated PE, the sensitivity of a pleural fluid PMN-E value equal to or greater than 230 µg/l was 0.64 and the specificity 0.81. Conclusions: Pleural fluid PMN-E was the marker that best differentiated infectious from non-infectious PE, and PMN-E values lower than 230 µg/l suggest non-infectious PE.

Metalloproteinases and tissue inhibitors of metalloproteinases in exudative pleural effusions

“…These findings concur with results from other studies and indicate that in infectious pleural effusions, particularly empyema, there is an intense inflammatory response and inhibition of fibrinolysis that would favour fibrin deposition [10,[12][13][14][15][16].…”

“…The inflammatory response initiated by the mesothelium provokes increased vascular patency and the release of inflammatory mediators, e.g. interleukin (IL)-8 and tumour necrosis factor alpha (TNF)-a [11][12][13], thereby favouring the formation of exudative pleural effusion, invasion of the pleural space by inflammatory cells and the release of neutrophil degranulation products, such as polymorphonuclear elastase (PMN-E) [14]. The fibrinolytic system is regulated by two plasminogen activators (PAs), tissue PA (t-PA) and urokinase PA (u-PA), and by plasminogen activator inhibitor type 1 (PAI-1) and 2 (PAI-2).…”

Pleural Involvement in Systemic Autoimmune Disorders

“…A number of studies have evaluated the clinical utility of several biomarkers to serve as noninvasive diagnostic tools and differentiate infectious from noninfectious pleural effusions. Although some of them seem to be promising [34, 35], their applicability is still in its infancy. Further studies are warranted to establish their usefulness.…”

Pleural-fluid myeloperoxidase in complicated and noncomplicated parapneumonic pleural effusions

“…Polymorphonuclear elastase (PMN-E), a protease that originates from azurophil granules of the polymorphonuclear leukocytes (neutrophils) in response to the release of inflammatory mediators, stands out among these [7]. The value of pleuralfluid PMN-E in the differentiation between infective and noninfective effusions has recently been established [8]. Myeloperoxidase (MPO) is a protein responsible for the peroxidase activity characteristic of the azurophilic granules and is essential for the oxidative mechanism of the phagocytes.…”