title: Repeated thoracenteses affect proinflammatory cytokines, vascular endothelial growth factor, and fibrinolytic activity in pleural transudates.
abstract: 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.
authors: Department of Chest Medicine, Taipei Medical University Hospital, School of Medicine, National Yang-Ming University, Taipei, Taiwan.
authors: Chi-Li
authors: CL
authors: Chung
authors: Ching-Yu
authors: CY
authors: Yeh
authors: Joen-Rong
authors: JR
authors: Sheu
authors: Yi-Chu
authors: YC
authors: Chen
authors: Shi-Chuan
authors: SC
authors: Chang
mesh_terms: 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*
chemical_list: 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