Abstract
Objective. To investigate the relationship among angiogenic cytokines, inflammatory markers, and fibrinolytic activity in tuberculous pleural effusion (TBPE) and their clinical importance. Methods. Forty-two patients diagnosed with TBPE were studied. Based on chest ultrasonography, there were 26 loculated and 16 nonloculated TBPE patients. The effusion size radiological scores and effusion vascular endothelial growth factor (VEGF), interleukin- (IL-) 8, plasminogen activator inhibitor type-1 (PAI-1), and tissue type plasminogen activator (tPA) were measured. Treatment outcome and pleural fibrosis, defined as radiological residual pleural thickening (RPT), were assessed at 6-month follow-up. Results. The effusion size and effusion lactate dehydrogenase (LDH), VEGF, IL-8, PAI-1, and PAI-1/tPA ratio were significantly higher, while effusion glucose, pH value, and tPA were significantly lower, in loculated than in nonloculated TBPE. VEGF and IL-8 correlated positively with LDH and PAI-1/tPA ratio and negatively with tPA in both loculated and nonloculated TBPE. Patients with higher VEGF or greater effusion size were prone to develop RPT (n = 14; VEGF, odds ratio 1.28, P = 0.01; effusion size, odds ratio 1.01, P = 0.02), and VEGF was an independent predictor of RPT in TBPE (receiver operating characteristic curve AUC = 0.985, P < 0.001). Conclusions. Effusion VEGF correlates with pleural inflammation and fibrosis and may be targeted for adjunct therapy for TBPE.
Highlights
Tuberculosis (TB) remains a major global public health issue and continues to cause significant morbidity and mortality worldwide [1]
Fibrin turnover in the pleural cavity is affected by fibrinolytic activity mediated by plasmin, which is regulated by the equilibrium between plasminogen activators (PAs) and plasminogen activator inhibitors (PAIs) [7]
The Scientific World Journal might play a role in the modulation of type plasminogen activator (tPA) and plasminogen activator inhibitor type-1 (PAI-1) [10] and that anti-vascular endothelial growth factor (VEGF) antibody could reduce fluid volume of inflammatory pleural effusion and attenuate pleural inflammation and fibrosis [11,12,13]. These findings suggest that VEGF may be involved in the regulation of inflammation, fibrin turnover and fluid loculation in the pleural cavity, and subsequent residual pleural thickening (RPT) or fibrosis [9], which was observed in our previous study on parapneumonic effusions [14]
Summary
Tuberculosis (TB) remains a major global public health issue and continues to cause significant morbidity and mortality worldwide [1]. Tuberculous pleural effusion (TBPE) is the most common form of extrapulmonary TB and often complicated with pleural fibrosis [2]. This pleural fluid is enriched in proteins, inflammatory cells, and various angiogenic cytokines [3], including vascular endothelial growth factor (VEGF) and interleukin- (IL-) 8, which stimulate migration of leukocytes, induce vascular hyperpermeability and pleural fluid production, activate coagulation cascade, and repress fibrinolytic activity within the pleural cavity [4, 5]. An imbalance between PAI-1 and tissue type plasminogen activator (tPA) may elicit fibrin gel formation in the pleural space and lead to pleural fluid loculation, fibrin neomatrix remodeling, and fibrosis [6, 8]
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