Repeated thoracenteses affect proinflammatory cytokines, vascular endothelial growth factor, and fibrinolytic activity in pleural transudates.
BACKGROUND
Repeated thoracenteses is indicated in patients with refractory, symptomatic transudative effusions. However, their effect on cytokines and fibrinolytic activity in pleural transudates remains unclear.


METHODS
Twenty-one patients with symptomatic, large amount of free-flowing transudative effusions caused by heart failure were studied. Thoracentesis with drainage of 500 mL of pleural fluid per day was done for 3 consecutive days (days 1 to 3). Pleural fluid characteristics, tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-8, vascular endothelial growth factor (VEGF), tissue-type plasminogen activator (tPA), and plasminogen activator inhibitor type 1 (PAI-1) were measured during each tap. Chest ultrasonography was done on day 6 to detect the fibrin strands in pleural effusion and the outcome of effusion was evaluated within 7 days after repeated thoracenteses.


RESULTS
Effusion levels of lactate dehydrogenase, neutrophils, TNF-alpha, IL-1 beta, IL-8, VEGF, and PAI-1 increased significantly during repeated thoracenteses. Furthermore, the values of PAI-1 and PAI-1/tPA obtained on days 2 and 3 were highly correlated with those of TNF-alpha, IL-1 beta, IL-8, and VEGF. On day 6, pleural fibrins were observed on chest ultrasonography in 6 patients (29%, fibrinous group) but were absent in the remaining 15 patients (nonfibrinous group). Compared with the nonfibrinous group, the effusion levels of TNF-alpha, IL-1 beta, VEGF, and PAI-1 on day 2 and day 3, and recurrence of symptomatic effusion after repeated thoracenteses were significantly higher in fibrinous group.


CONCLUSIONS
Repeated thoracenteses may induce local release of proinflammatory cytokines, VEGF and PAI-1, which may result in fibrin deposition and impair resolution of pleural transudates.
Chung
Chi-Li
CL
Department of Chest Medicine, Taipei Medical University Hospital, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
Yeh
Ching-Yu
CY
Sheu
Joen-Rong
JR
Chen
Yi-Chu
YC
Chang
Shi-Chuan
SC
D000368:Aged; D000369:Aged, 80 and over; D002452:Cell Count; D016207:Cytokines / Q000378:metabolism*; D004912:Erythrocytes / Q000473:pathology; D005260:Female; D005337:Fibrin / Q000378:metabolism; D005342:Fibrinolysis / Q000502:physiology*; D005947:Glucose / Q000378:metabolism; D006333:Heart Failure / Q000150:complications; D006801:Humans; D006863:Hydrogen-Ion Concentration; D053583:Interleukin-1beta / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D007962:Leukocytes / Q000473:pathology; D008168:Lung / Q000378:metabolism / Q000473:pathology; D008297:Male; D019152:Paracentesis / Q000009:adverse effects*; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis / Q000378:metabolism; D010996:Pleural Effusion / Q000209:etiology / Q000378:metabolism* / Q000601:surgery; D019233:Retreatment / Q000009:adverse effects; D010959:Tissue Plasminogen Activator / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*
D016207:Cytokines; D053583:Interleukin-1beta; D017395:Plasminogen Activator Inhibitor 1; C051321:SERPINE1 protein, human; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; D005337:Fibrin; D007770:L-Lactate Dehydrogenase; D010959:Tissue Plasminogen Activator; D005947:Glucose