Coagulation Factors and Fibrinogen in Pleural Effusions

Glauser, Frederick L.; Otis, Peter T.; Levine, Richard I.; Smith, William R.

doi:10.1159/000193755

Cited by 15 publications

(11 citation statements)

References 2 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This fluid has many characteristics of a plasma ultrafiltate with a protein concentration of 1-3 g/dL. Although albumin is the principal protein species in pleural fluid, fibrinogen and other coagulation proteins including prothrombin and factors V, VII, VIII, IX, X, XI, XII, and XIII are present (19). If TF expression by the pleura were constitutive as previously suggested (8), one would expect some degree of fibrin deposition to be detectable on normal mesothelium.…”

Section: Discussionmentioning

confidence: 92%

“…However, in other cell types, such as quiescent fibroblasts, TF expression is not constitutive but can be induced by exposure to serum (12)(13)(14) or various cytokines (15)(16)(17)(18). Since all the soluble, plasma-derived coagulation factors are normally present in pleural fluid (19), constitutive TF expression by HMC would be expected to promote fibrin deposition, even in the absence of disease. For example, increased vascular permeability alone is reported to cause fibrin deposition in skin and muscle tissues (20).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Tissue Factor Expression in Mesothelial Cells: Induction BothIn VivoandIn Vitro

Bottles

Lászik

Morrissey

et al. 1997

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

Exudative pleural effusions are characterized by a high protein content and frequently progress to loculation and fibrosis. To test the hypothesis that tissue factor (TF) plays an integral role in this process, we investigated the expression of TF by human mesothelial cells (HMC) both in vivo and in vitro, and measured the effect of serum on HMC expression of TF in vitro. In vivo TF expression was not detected in HMC of normal pleura, but was detected in HMC of pleura overlying inflamed lung. In vitro, quiescent HMC demonstrated negligible levels of TF expression; however, upon serum stimulation there was a marked induction in both TF protein level and activity, peaking at 8-9 h. In contrast, treating quiescent HMC with plasma resulted in a further small, but significant, decrease in TF expression. This serum-induced rise in TF was also reflected in TF mRNA levels and did not require de novo protein synthesis. These results suggest that induction of HMC TF expression may be important in triggering both the intrapleural activation of prothrombin and the deposition of fibrin characteristic of inflammatory effusions.

show abstract

Section: Discussionmentioning

confidence: 92%

mentioning

confidence: 99%

Tissue Factor Expression in Mesothelial Cells: Induction BothIn VivoandIn Vitro

Bottles

Lászik

Morrissey

et al. 1997

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

show abstract

“…In the pathological state, pleural fluid accumulates within the thoracic cavity when more fluid enters the pleural space than is removed [ 49 , 50 ]. Therefore, pleural fluid, which has traditionally been regarded by physicians as an inert fluid, contains all of the proteins/enzymes that are present in plasma, including those that participate in coagulation and fibrinolysis [ 39 ]. Plasma coagulation-relevant proteins in pleural fluids are no longer contained in their natural environment (i.e.…”

Section: Discussionmentioning

confidence: 99%

Hemostatic findings of pleural fluid in dogs and the association between pleural effusions and primary hyperfibrino(geno)lysis: A cohort study of 99 dogs

et al. 2018

View full text Add to dashboard Cite

The primary objective of this study was to determine if activation of coagulation and fibrinolysis occurs in canine pleural effusions. Thirty-three dogs with pleural effusions of different origin were studied. Pleural effusion fibrinogen concentrations were significantly lower, while pleural fibrin-fibrinogen degradation products (FDPs) and D-dimer concentrations were significantly higher than those in plasma (P < 0.001 for all comparisons). These results show that, in canine pleural fluids, there is evidence of coagulation activation and fibrinolysis. The secondary aims of the current study were to determine if primary hyperfibrinolysis ([PHF] i.e., elevated plasma FDPs with a normal D-dimer concentrations), occurs in dogs with pleural effusion, and whether the presence of a concurrent inflammatory process may have activated the hemostatic cascade, with its intrinsically linked secondary hyperfibrinolysis, masking the concurrent PHF. The previously 33 selected dogs with pleural effusion (group 1) were compared to two control groups of 33 healthy (group 2) and 33 sick dogs without pleural effusion (group 3). Serum fibrinogen, FDPs, D-dimer, C-reactive protein (CRP), fibrinogen/CRP ratio, and frequency of PHF were determined. Fibrinogen, FDPs, D-dimer and CRP concentrations in group 1 were significantly increased compared to group 2 (P < 0.001 for all comparisons). FDPs and CRP concentrations in group 1 were also significantly increased compared to group 3 (P = 0.001 and P < 0.001, respectively). The fibrinogen/CRP ratio was significantly decreased in group 1 compared to groups 2 and 3 (P < 0.001 for both comparison). The frequency of PHF was significantly higher in group 1 compared to groups 2 (P = 0.004), but not compared to group 3. These results support the hypothesis that PHF occurs significantly more often in dogs with pleural effusion compared to healthy dogs. Nevertheless, the decrease in the fibrinogen/CRP ratio in group 1 compared to group 3, considering the higher FDPs and similar D-dimer concentrations, would suggest that PHF is also more frequent in dogs with pleural effusion compared to sick control dogs, and that this phenomenon is hidden due to concurrent secondary hyperfibrinolysis.

show abstract

“…Pleural inflammation leads to increased microvascular permeability with formation of exudative effusions that contain plasma constituents. Albumin is the principal protein present in exudative pleural effusions, but coagulation and fibrinolytic proteins are also well represented in pleural effusions [4,[10][11][12][13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Plasmin enhances cell surface tissue factor activity in mesothelial and endothelial cells

Kothari

Kaur

Sahoo

et al. 2009

Journal of Thrombosis and Haemostasis

View full text Add to dashboard Cite

Summary. Background: Mesothelial cells that line the thoracic cavity play an important role in maintaining the local balance between procoagulant and fibrinolytic activity, a role akin to the endothelial cells in blood vessels. The mechanism(s) responsible for increased tissue factor (TF) expression in mesothelial cells in response to injury are at present unclear. Objective: To investigate whether plasmin or thrombin, two major proteases that may be generated on the pleural surface upon injury, induce TF expression in human pleural mesothelial cells (HMC) and elucidate the underlying mechanism(s). Methods: Confluent monolayers of HMC and human umbilical vein endothelial cells (HUVEC) were exposed to plasmin or thrombin for varying time periods and TF expression was analyzed by measuring its activity in a factor Xa generation assay, TF antigen levels by immunoblot analysis and TF mRNA by Northern blot analysis. Results: Both plasmin and thrombin treatments increased cell surface TF activity in HMC by 3-to 4-fold. In contrast to thrombin, plasmin-induced TF activity is not dependent on the de novo synthesis of TF. In HUVEC, plasmin had a minimal effect on unperturbed HUVEC whereas it markedly increased TF activity of activated HUVEC. Plasmin treatment neither affected anionic phospholipid levels at the cell surface nor released protein disulfide isomerase, an oxidoreductase protein that was newly described to play a role in TF activation. Plasmin cleaved cell-associated TFPI. Conclusion: Thrombin up-regulates TF activity in HMC through the transcriptional activation of TF whereas plasmin increases TF activity by inactivating the cell-associated TFPI by a limited proteolysis.

show abstract

Coagulation Factors and Fibrinogen in Pleural Effusions

Cited by 15 publications

References 2 publications

Tissue Factor Expression in Mesothelial Cells: Induction BothIn VivoandIn Vitro

Tissue Factor Expression in Mesothelial Cells: Induction BothIn VivoandIn Vitro

Hemostatic findings of pleural fluid in dogs and the association between pleural effusions and primary hyperfibrino(geno)lysis: A cohort study of 99 dogs

Plasmin enhances cell surface tissue factor activity in mesothelial and endothelial cells

Contact Info

Product

Resources

About