Proteases and antiproteases related to the coagulation system in plasma and ascites

Hemostatic Findings in Ascitic Fluid: A Cross‐Sectional Study in 70 Dogs

“…Third, a study of 23 plasma proteins revealed that only fibrinogen and plasminogen had a lower concentration than expected in the ascitic fluid, suggesting an accelerated degradation of these proteins in plasmin and FDPs after the activation of the fibrinolytic system within this fluid . The activation of the plasminogen in the ascitic fluid is due to the presence of tissue plasminogen activator, urinary plasminogen activator, or both enzymes which can be released (from a preformed storage pool) or leak in the ascitic fluid (following the damage induced by the disease causing the ascites formation) from the mesothelial and submesothelial endothelium cells . Finally, in support of the fibrinolytic activity of the ascitic fluid, there is also the evidence of primary hyperfibrinolysis in ascitic human patients treated with palliative peritoneovenous shunts after the reinfusion of their abdominal fluid in the systemic circulation …”

“…5 The activation of the plasminogen in the ascitic fluid is due to the presence of tissue plasminogen activator, urinary plasminogen activator, or both enzymes which can be released (from a preformed storage pool) or leak in the ascitic fluid (following the damage induced by the disease causing the ascites formation) from the mesothelial and submesothelial endothelium cells. 5,[21][22][23][24][25][26][27] Finally, in support of the fibrinolytic activity of the ascitic fluid, there is also the evidence of primary hyperfibrinolysis in ascitic human patients treated with palliative peritoneovenous shunts after the reinfusion of their abdominal fluid in the systemic circulation. 23,26,[28][29][30] Primary hyperfibrinolysis, also sometimes named primary hyperfibrinogenolysis, 31,32 is a rare condition that occurs when the generation of plasmin within the general circulation (plasminemia) exceeds the neutralizing capacity of the antiplasmins.…”

“…5,[21][22][23][24][25][26][27] Finally, in support of the fibrinolytic activity of the ascitic fluid, there is also the evidence of primary hyperfibrinolysis in ascitic human patients treated with palliative peritoneovenous shunts after the reinfusion of their abdominal fluid in the systemic circulation. 23,26,[28][29][30] Primary hyperfibrinolysis, also sometimes named primary hyperfibrinogenolysis, 31,32 is a rare condition that occurs when the generation of plasmin within the general circulation (plasminemia) exceeds the neutralizing capacity of the antiplasmins. 33 In humans, this has been reported in association with acute conditions, such as shock, 31 surgical procedures, 34 liver transplantation, 35 acute leukemia, 36 or the administration of thrombolytic drugs.…”

Proteases and antiproteases related to the coagulation system in plasma and ascites — Influence of dexamethasone

“…A m o n g the patients not showing an increase was one with malignant ascites due to an u n k n o w n t u m o r with peritoneal carcinomatosis, one with Budd-Chiari syndrome, and three with alcoholic cirrhosis. In three of the ten ascites retransfusion procedures a level o f 0.7 C T A U / m l plasminogen in ascites was not reached prior to the procedure and signs of fibrinolysis [14] occurred. Interestingly, in the patient with Budd-Chiari s y n d r o m e (patient 8), three different time courses were seen (Table 1).…”

“…We have previously shown that coagulation disorders induced by ascites retransfusion are probably mediated by the infusion of plasminogen activators from ascites into the circulation [14]. It has been reported that peritoneal macrophages synthesize and release plasminogen activators [2,7,16], and that this phenomenon is stimulated by endotoxin [6].…”