Abstract
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.
Highlights
Fibrinolysis is the process whereby stable fibrin strands are broken down by plasmin [1]
The decrease in the fibrinogen/C-reactive protein (CRP) ratio in group 1 compared to group 3, considering the higher fibrinogen degradation products (FDPs) and similar D-dimer concentrations, would suggest that Primary hyperfibrinolysis (PHF) is more frequent in dogs with pleural effusion compared to sick control dogs, and that this phenomenon is hidden due to concurrent secondary hyperfibrinolysis
We have shown that pleural effusions have fibrinolytic activity independent of the underlying mechanism of intra-thoracic fluid accumulation, and we demonstrated that almost 40% of these dogs have systemic coagulative alterations suggesting PHF
Summary
Fibrinolysis is the process whereby stable fibrin strands are broken down by plasmin [1]. Besides an excessive serum plasmin concentration, other enzymes such as serum tryptase or non-plasmic polymorphonuclear elastase have been reported as possible causes of PHF, when their serum concentration overwhelms the neutralizing capacity of the antiplasmins [8,9,10]. In humans, this has been associated with acute conditions, such as surgical procedures [11], shock [4], liver transplantation [12], acute leukaemia [13], or treatment with thrombolytic drugs. Because “cross-talk” between the inflammatory and hemostatic systems may be responsible for the activation of hemostasis associated with systemic inflammation [20,21], secondary or “reactive” hyperfibrinolysis, is often present in patients with inflammatory diseases
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