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Effect of Repeated Thoracenteses on Fibrinolytic Activity in Malignant Pleural EffusionEffect of Repeated Thoracenteses on Fibrinolytic Activity in Malignant Pleural Effusion FREE TO VIEW

Hiroichi Ishikawa, MD; Hiroaki Satoh, MD; Kiyohisa Sekizawa, MD
Author and Funding Information

Affiliations: University of Tsukuba, Ibaraki, Japan,  Taipei Medical University, Taipei, Taiwan, Republic of China,  National Yan-Ming University, Taipei, Taiwan, Republic of China

Correspondence to: Hiroaki Satoh, MD, Division of Respiratory Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba-city, Ibaraki, 305-8575, Japan; e-mail: hirosato@md.tsukuba.ac.jp



Chest. 2004;125(5):1965-1966. doi:10.1378/chest.125.5.1965
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To the Editor:

We read with interest the report by Chung and associates1(April 2003) on the effect of repeated thoracenteses on fluid characteristics, cytokines, and fibrinolytic activity in malignant pleural effusion. We also studied and published an article on the fibrinolytic activity in pleural effusion.2

From their results, the authors described that the “values of PAI-1 [plasminogen activator inhibitor-1] in pleural fluid increased gradually during repeated thoracenteses and were significantly higher on day 2 and day 3 than on day 1.” However, according to their Figure, there seems to be no significant difference between PAI-1 levels on day 2 and day 3, even though the same procedure of thoracenteses were repeated. Did repeated thoracenteses truly influence of the PAI-1 levels in pleural fluid? The authors also showed that “repeated thoracenteses had no effect on the effusion levels of tPA [tissue-type plasminogen activator].” From the results of our previous study2, we speculated that both urokinase-type plasminogen activators and tPAs and their inhibitors had some roles in the formation of pleural effusion, and the balance of them might be important for fibrinolytic activity in malignant pleural effusion. We appreciate hearing from the authors whether evaluate tPA had no relationship to pleural inflammation, which was caused by repeated thoracenteses and the fibrinolytic activity in malignant pleural effusion.

Chung, CL, Chen, YC, Chang, SC (2003) Effect of repeated thoracenteses on fluid characteristics, cytokines, and fibrinolytic activity in malignant pleural effusion.Chest123,1188-1195. [CrossRef] [PubMed]
 
Ishikawa, H, Satoh, h, Hasegawa, S, et al Urokinase-type plasminogen activator in carcinomatous pleural fluid.Eur Respir J1997;10,1566-1571. [CrossRef] [PubMed]
 

Effect of Repeated Thoracenteses on Fibrinolytic Activity in Malignant Pleural Effusion

To the Editor:

We would like to reply to the comments on our article (April 2003)1 by Satoh and colleagues. They commented that repeated thoracenteses did not influence the effusion levels of plasminogen activator inhibitor (PAI)-1 in patients with malignant pleural effusion. Furthermore, they suggested that both urokinase-type and tissue-type plasminogen activators (PAs) and their inhibitors (ie, PAIs) have some role in the formation of pleural effusions, and that their balance may be important for fibrinolytic activity in malignant effusions.

We agree that PA and PAI may be involved in the formation of pleural effusions, and that the balance between PA and PAI is important for fibrinolytic activity in malignant and inflammatory pleural effusions.23 In terms of the formation of pleural effusions, however, the size of the role played by fibrinolytic enzymes in the pleural cavity remains speculative and deserves further study for verification.

In our original article,1 the patients with malignant pleural effusions were divided into fibrinous and nonfibrinous groups, according to the amount of fibrin formation on day 6, after 3 days of repeated thoracenteses. Compared to the effusion levels of PAI-1 on day 1, those on days 2 and 3 increased significantly in the 26 patients studied (see Table 2 in the article), and in particular in patients in the fibrinous group (see Table 3 and Fig 1 in the article). By contrast, repeated thoracenteses did not affect the effusion levels of PAI-1 in patients in the nonfibrinous group. These findings highlight the fact that fibrinolytic activity in malignant pleural effusions may vary widely, and that the response of the pleura to repeated thoracenteses differs greatly in patients with malignant pleural effusions.

Satoh and colleagues thought that the effusion levels of PAI-1 on days 2 and 3 were comparable, and concluded that repeated thoracenteses did not affect the levels of PAI-1 in malignant pleural effusions. However, this is not the case. During repeated thoracenteses, the effusion levels of PAI-1 on day 2 increased significantly and remained at high levels on day 3, compared with day 1. Similarly, the effusion levels of tumor necrosis factor (TNF)-α increased significantly on day 2 and remained at high levels on day 3, compared with day 1 (see Tables 2 and 3, and Fig 1 in the article). Furthermore, the effusion levels of PAI-1 and TNF-α seen on days 2 and 3 were significantly higher in the fibrinous group than in the nonfibrinous group (see Table 3 and Fig 1 in the article). These results indicated that repeated thoracenteses increased the effusion levels of PAI-1 in patients with malignant pleural effusions, and that the increase in effusion levels of PAI-1 during repeated thoracenteses might be due to the enhanced local release of TNF-α. By contrast, the effusion levels of tissue type plasminogen activator (tPA) and the PAI-1/tPA ratio showed no significant changes during repeated thoracenteses in patients with malignant pleural effusions, either as a whole or further divided into fibrinous and nonfibrinous groups. Based on these results, it seems that the role, if any, of tPA in fibrin formation after repeated thoracenteses was limited.

Taken together, repeated thoracenteses may cause pleural inflammation and may induce the local release of proinflammatory cytokines such as TNF-α, which may subsequently cause an imbalance in levels of PAI-1 and tPA, and may lead to fibrin formation. The imbalance of PAI-1 and tPA levels that was induced by repeated thoracenteses in malignant pleural effusions was due mainly to the enhanced release of PAI-1, and not to the changes in tPA levels. Further studies are needed to verify whether repeated thoracenteses can be used as a model of pleural injury and/or pleural inflammation, and to explore the roles of PAI and PA in this issue.

References
Chung, CL, Chen, YC, Chang, SC Effect of repeated thoracenteses on fluid characteristics, cytokines, and fibrinolytic activity in malignant effusions.Chest2003;123,1188-1195. [CrossRef] [PubMed]
 
Philip-Jot, F, Alessi, MC, Philip-Jot, C, et al Fibrinolytic and inflammatory processes in pleural effusions.Eur Respir J1995;8,1352-1356. [CrossRef] [PubMed]
 
Hua, CC, Chang, LC, Chen, YC, et al Proinflammatory cytokines and fibrinolytic enzymes in tuberculous and malignant pleural effusions.Chest1999;116,1292-1296. [CrossRef] [PubMed]
 

Figures

Tables

References

Chung, CL, Chen, YC, Chang, SC (2003) Effect of repeated thoracenteses on fluid characteristics, cytokines, and fibrinolytic activity in malignant pleural effusion.Chest123,1188-1195. [CrossRef] [PubMed]
 
Ishikawa, H, Satoh, h, Hasegawa, S, et al Urokinase-type plasminogen activator in carcinomatous pleural fluid.Eur Respir J1997;10,1566-1571. [CrossRef] [PubMed]
 
Chung, CL, Chen, YC, Chang, SC Effect of repeated thoracenteses on fluid characteristics, cytokines, and fibrinolytic activity in malignant effusions.Chest2003;123,1188-1195. [CrossRef] [PubMed]
 
Philip-Jot, F, Alessi, MC, Philip-Jot, C, et al Fibrinolytic and inflammatory processes in pleural effusions.Eur Respir J1995;8,1352-1356. [CrossRef] [PubMed]
 
Hua, CC, Chang, LC, Chen, YC, et al Proinflammatory cytokines and fibrinolytic enzymes in tuberculous and malignant pleural effusions.Chest1999;116,1292-1296. [CrossRef] [PubMed]
 
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