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Chi-Li Chung, MD, MS*; Ching-Yu Yeh, MD; Joen-Rong Sheu, PhD; Yi-Chu Chen, BS; Shi-Chuan Chang, MD, PhD
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Taipei Medical University Hospital, Taipei Medical University, Taipei, Taiwan ROC

Chest. 2006;130(4_MeetingAbstracts):142S. doi:10.1378/chest.130.4_MeetingAbstracts.142S-b
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PURPOSE: Repeated thoracenteses may induce fibrinogenesis in malignant effusions. In this study, we investigated effect of repeated thoracenteses on fibrinogenesis in pleural transudates.

METHODS: Twenty-seven patients with symptomatic, large amount of free-flowing transudative effusions were studied. Thoracentesis with drainage of 500 mL was done for 3 consecutive days (days 1 to 3). Pleural pressure, pleural elastance (PE, the decline of pleural pressure [cm H2O] divided by amount of effusion removed [liter]), and pleural fluid characteristics, tumor necrosis factor(TNF)-α, interleukin(IL)-1β, IL-6, IL-8, vascular endothelial growth factor (VEGF), tissue type plasminogen activator and plasminogen activator inhibitor type 1 (PAI-1) were measured during each tap. Chest ultrasonography was done before each tap and on day 6 to detect fibrin in pleural effusion.

RESULTS: Pleural fluid lactate dehydrogenase, total leukocytes, neutrophils, TNF-α, IL-1β, IL-6, IL-8, VEGF and PAI-1 increased significantly during repeated thoracenteses, and the increases of effusion PAI-1 (day 2 minus day 1 and day 3 minus day 2) were highly correlated with those of TNF-α (r = 0.52, p = 0.005 and r = 0.47, p = 0.01, respectively), IL-6 (r = 0.45, p = 0.01 and r = 0.47, p = 0.01, respectively), IL-8 (r = 0.42, p = 0.02 and r = 0.51, p = 0.006, respectively) and VEGF (r = 0.53, p = 0.004 and r = 0.44, p=0.02, respectively). On day 6, fibrins were observed in pleural effusion in 7 patients (26%, fibrinous group) but were absent in the remaining 20 patients (74%, nonfibrinous group). Compared to nonfibrinous group, PE and effusion VEGF at first tap were significantly higher in fibrinous group (p = 0.002 and p = 0.03, respectively).

CONCLUSION: Repeated thoracenteses may cause pleura inflammation and induce local release of proinflammatory cytokines, chemokines and VEGF, which in turn enhance the release of PAI-1 and lead to fibrin generation and deposition.

CLINICAL IMPLICATIONS: Initial PE and effusion VEGF may be of value in predicting fibrinogenesis in transudative effusions following repeated thoracenteses.

DISCLOSURE: Chi-Li Chung, None.

Tuesday, October 24, 2006

2:30 PM - 4:00 PM




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