Pleural Fibrinolytic Activity Is Decreased in Inflammation as Demonstrated in Quinacrine Pleurodesis Treatment of Malignant Pleural Effusion

Agrenius, Veronica; Chmielewska, Joanna; Widström, O; Blombäck, Margareta

doi:10.1164/ajrccm/140.5.1381

Cited by 52 publications

(43 citation statements)

References 13 publications

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“…The interactions between inflammation and coagulation-fibrinolysis balance in the pleural space described by us and others [25,26,33], taken together with the finding of elevated levels of IL-8 in plasma of up to 44% of our patients in the present study, would suggest that after application of the pleurodesis agent IL-8 could disseminate from the inflamed pleural space into the bloodstream, thus activating the systemic coagulation. The association found between high levels of IL-8 in plasma and short survival ( fig.…”

Section: Discussionsupporting

confidence: 78%

Interleukin-8 activates coagulation and correlates with survival after talc pleurodesis

Montes-Worboys¹,

Rodriguez-Portal²,

Arellano-Orden³

et al. 2009

European Respiratory Journal

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The aim of our study was to investigate whether interleukin (IL)-8 activates systemic coagulation after talc pleurodesis in malignant pleural effusion (MPE), and whether levels of IL-8 in plasma are related to early death after talc pleurodesis.IL-8 and tumour necrosis factor (TNF)-a were measured in samples from 231 MPE patients before and after talc pleurodesis. Whole blood from 31 healthy volunteers was incubated with IL-8, TNF-a and thromboplastin for 3 h in vitro, and thrombin-antithrombin (TAT) levels were measured. The same stimulation of blood samples was repeated using doses of calibrated talc.Nine, 12 and 17 patients died within 7, 10 and 15 days respectively. IL-8 was elevated in 102 patients within 48 h, and thrombotic events were observed in six of those patients. Survival correlated inversely with IL-8 at 24 and 48 h, and a significant correlation was also found between IL-8 and TAT. A positive dose-dependent correlation with TAT production was observed when blood was stimulated with IL-8 in vitro. However, there was no significant response to stimulation with talc, as compared with control blood samples.IL-8 is involved in the activation of coagulation that may occur after talc pleurodesis, and might also be implicated in early death of patients with MPE.

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Section: Discussionsupporting

confidence: 78%

Interleukin-8 activates coagulation and correlates with survival after talc pleurodesis

Montes-Worboys¹,

Rodriguez-Portal²,

Arellano-Orden³

et al. 2009

European Respiratory Journal

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“…The fibrinolytic system in pleural fluids was first studied by AGRENIUS et al [20], who showed that PAI-1 plays an important role in the regulation of fibrinolysis. We have previously studied the levels of tissue-type plasminogen activator (t-PA) and PAI-1 in pleural fluids, and demonstrated that not only in malignant but also in inflamed exudates those levels were higher than those in transudates due to CHF [9].…”

Section: Discussionmentioning

confidence: 99%

“…The complete response rate (48%) in this study using OK-432 as sclerosing agent, was disappointing as compared to the results with other agents commonly used in the United States or Europe, such as tetracycline, talc or bleomycin. Since the levels of u-PA were only examined in carcinomatous pleuritis due to pulmonary adenocarcinoma, our conclusions might not be applied to other types of lung cancer or to pleural metastasis of Recently, there have been other reports concerning the relationship between the fibrinolytic system and chemical pleurodesis or pleural symphysis [10,20]. RODRIGUEZ-PANADERO et al [24] demonstrated that increased pleural fibrinolytic activity, as expressed by D-dimer levels, is associated with failure of pleurodesis, despite significant inhibitory activity of PAI [24].…”

Section: Discussionmentioning

confidence: 99%

Urokinase-type plasminogen activator in carcinomatous pleural fluid

Ishikawa

Satoh²,

Hasegawa³

et al. 1997

Eur Respir J

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Urokinase-type plasminogen activator (u-PA) is known to be secreted by malignant cells during proliferation and migration, and is associated with tumour cell invasion and metastasis. This study was undertaken to evaluate whether u-PA is significantly increased in carcinomatous pleural fluids compared to those due to other aetiologies, and to identify the cells in the pleural space that are involved in its accumulation.Using an enzyme-linked immunosorbent assay, we quantified u-PA in the pleural fluid specimens of 40 patients with carcinomatous pleuritis, 18 with tuberculosis, 18 with parapneumonic pleuritis and 11 with congestive heart failure (CHF).The level of u-PA was elevated in carcinomatous pleural fluid compared with the level in transudative pleural fluid from patients with CHF (p<0.0001). The levels of u-PA were not statistically different between patients with cancer and tuberculosis, or between patients with cancer and pneumonia. The levels of u-PA in patients who did not respond to chemical pleurodesis were significantly higher than those who had complete response (p=0.0001). In immunocytochemical and immunoblotting studies, cancer cells in pleural fluids as well as mesothelial cells contained u-PA. u-PA was detected in the culture supernatants of viable pleural cells in the majority of patients with carcinomatous pleuritis.Our results suggest that local release of urokinase-type plasminogen activator by viable cells, including cancer cells and mesothelial cells, may affect the levels of urokinase-type plasminogen activator in pleural fluids. Eur Respir J 1997; 10: 1566-1571

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“…Intrapleural hypofibrinolysis, due mainly to excessive concentration of inhibitors, has been postulated in these patients [2]. Conversely, D dimer (D-D) level, a marker of solid phase fibrin dissolution was found to be high in patients with malignant effusion, suggesting local fibrinolysis activation [4].…”

mentioning

confidence: 99%

Fibrinolytic and inflammatory processes in pleural effusions

Philip-Joët¹,

Alessi²,

Philip-Joet³

et al. 1995

Eur Respir J

103

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F Fi ib br ri in no ol ly yt ti ic c a an nd d i in nf fl la am mm ma at to or ry y p pr ro oc ce es ss se es s i in n p pl le eu ur ra al l e ef ff fu us si io on ns s F. Philip-Joët*, M-C. Alessi**, C. Philip-Joët**, M. Aillaud**, J-R. Barriere*, A. Arnaud*, I. Juhan-Vague** Sixty patients with pleural effusion were studied. The underlying aetiology was empyema in 10 cases, tuberculosis in 9, cancer in 31, cardiac failure in 7, and undetermined in 3. Plasminogen, plasminogen activator inhibitor 1 (PAI-1) and 2 (PAI-2), tissue type plasminogen activator (t-PA), urokinase (u-PA) and D-dimers (D-D) were quantified in plasma samples and pleural effusion specimens. These data were then correlated with inflammatory or infectious parameters, i.e. fibrinogen, von Willebrand factor (vWF), erythrocyte sedimentation rate (ESR), protein concentration, and white blood cell count.D-D levels were higher in pleural fluid than in plasma. D-D levels were not correlated with either plasminogen activator or plasminogen activator inhibitor levels, suggesting the presence of other fibrinolytic pathways. PAI levels (PAI activity, PAI-1 antigenicity, PAI-2 antigenicity) and vWF levels were significantly higher in patients with tuberculosis and empyema than in patients with cancer or cardiac failure. Regression analysis between inflammatory and fibrinolytic parameters showed that pleural PAI levels were significantly correlated with pleural neutrophil count, vWF levels, and plasma fibrinogen levels. D-D levels were correlated with blood ESR. No significant difference in pleural t-PA, u-PA and D-D levels was observed between aetiologies. The highest pleural t-PA and u-PA values were noted in patients with cancer, especially lymphoma. Plasma t-PA levels were higher in patients with pleural effusion secondary to congestive heart failure, but this difference did not reach statistical significance.In conclusion, pleural PAI levels are related to polymorphonuclear count and vWF levels, i.e. to inflammatory processes. Elevated levels of plasminogen activators suggest a possible role in some malignant pleural diseases.

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Pleural Fibrinolytic Activity Is Decreased in Inflammation as Demonstrated in Quinacrine Pleurodesis Treatment of Malignant Pleural Effusion

Cited by 52 publications

References 13 publications

Interleukin-8 activates coagulation and correlates with survival after talc pleurodesis

Interleukin-8 activates coagulation and correlates with survival after talc pleurodesis

Urokinase-type plasminogen activator in carcinomatous pleural fluid

Fibrinolytic and inflammatory processes in pleural effusions

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