scholarly journals Serial studies of protein C and its plasma inhibitor in patients with disseminated intravascular coagulation

Blood ◽  
1985 ◽  
Vol 66 (1) ◽  
pp. 59-63
Author(s):  
RA Marlar ◽  
J Endres-Brooks ◽  
C Miller
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Protein C ◽  
Fatal Case ◽  
Plasma Samples ◽  
Normal Range ◽  
C Protein ◽  
Intravascular Coagulation ◽  
Protein C Inhibitor ◽  
Serial Samples ◽  
Protein C Activity

This study was undertaken to determine the levels of protein C antigen and activity and protein C inhibitor in sequential plasma samples of disseminated intravascular coagulation (DIC) patients. Our normal range for both protein C antigen and activity is 70 to 130 U/dL, and protein C inhibitor is 65 to 135 U/dL. A decreased level of protein C activity was found in 96% of the plasma samples from individuals with DIC; the protein C antigen was decreased in 73%. The inhibitor of protein C was decreased in all samples. Analysis of serial samples from patients with DIC reveals that protein C activity and antigen and protein C inhibitor decrease progressively during the initial stages of DIC and remain at a low level for 24 to 48 hours before gradually returning toward normal in nonfatal cases. The protein C activity decreases in parallel with protein C inhibitor and is lower than protein C antigen. In a fatal case of DIC, protein C activity and protein C inhibitor rapidly decreased to undetectable levels; however, protein C antigen was gradually decreasing but still detectable at time of death. In DIC, a discrepancy initially occurs between the activity and antigen of protein C, suggesting a complex with the inhibitor or other inactive forms of protein C. Protein C appears to play a major role in the control of DIC.

scholarly journals Serial studies of protein C and its plasma inhibitor in patients with disseminated intravascular coagulation

Blood ◽  
1985 ◽  
Vol 66 (1) ◽  
pp. 59-63 ◽  
Author(s):  
RA Marlar ◽  
J Endres-Brooks ◽  
C Miller
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Protein C ◽  
Fatal Case ◽  
Plasma Samples ◽  
Normal Range ◽  
C Protein ◽  
Intravascular Coagulation ◽  
Protein C Inhibitor ◽  
Serial Samples ◽  
Protein C Activity

Abstract This study was undertaken to determine the levels of protein C antigen and activity and protein C inhibitor in sequential plasma samples of disseminated intravascular coagulation (DIC) patients. Our normal range for both protein C antigen and activity is 70 to 130 U/dL, and protein C inhibitor is 65 to 135 U/dL. A decreased level of protein C activity was found in 96% of the plasma samples from individuals with DIC; the protein C antigen was decreased in 73%. The inhibitor of protein C was decreased in all samples. Analysis of serial samples from patients with DIC reveals that protein C activity and antigen and protein C inhibitor decrease progressively during the initial stages of DIC and remain at a low level for 24 to 48 hours before gradually returning toward normal in nonfatal cases. The protein C activity decreases in parallel with protein C inhibitor and is lower than protein C antigen. In a fatal case of DIC, protein C activity and protein C inhibitor rapidly decreased to undetectable levels; however, protein C antigen was gradually decreasing but still detectable at time of death. In DIC, a discrepancy initially occurs between the activity and antigen of protein C, suggesting a complex with the inhibitor or other inactive forms of protein C. Protein C appears to play a major role in the control of DIC.

Behaviour of Protein C Inhibitor in Intravascular Coagulation and Liver Disease

1984 ◽  
Vol 52 (01) ◽  
pp. 071-074 ◽  
Author(s):  
R B Francis ◽  
W Thomas
Keyword(s):  
Liver Disease ◽  
Protein C ◽  
Normal Subjects ◽  
Hepatic Necrosis ◽  
Functional Assay ◽  
Normal Range ◽  
Intravascular Coagulation ◽  
Hemostatic System ◽  
Protein C Inhibitor ◽  
Protein C Activity

SummaryWe measured levels of protein C inhibitor in patients with disseminated intravascular coagulation (DIC) and liver disease using a functional assay. Levels in 24 normal subjects averaged 93% of the amount in normal pooled plasma, giving a normal range of 65 to 121%. Levels were below normal in 8 of 17 patients with DIC, in 4 of 19 patients with liver cirrhosis, and in 3 patients with acute hepatic necrosis. Levels were normal or elevated in 9 of 10 patients with cirrhosis and accelerated fibrinolysis, and in 6 patients receiving warfarin. We conclude that protein C inhibitor may be involved in regulation of protein C activity during pathologic activation of the hemostatic system (DIC). Decreased protein C inhibitor does not appear to contribute to the pathogenesis of accelerated fibrinolysis in liver disease. The liver may be the site of synthesis of protein C inhibitor.

scholarly journals Protein C activity value as a prognostic factor in sepsis-induced disseminated intravascular coagulation

2014 ◽  
Vol 21 (6) ◽  
pp. 614-622
Author(s):  
Toshihiro Sakurai ◽  
Shu Yamada ◽  
Maki Kitada ◽  
Satoshi Hashimoto ◽  
Shoko Hashimoto ◽  
...  
Keyword(s):  
Prognostic Factor ◽  
Disseminated Intravascular Coagulation ◽  
Protein C ◽  
Intravascular Coagulation ◽  
Protein C Activity

Activation of Protein C and Its Distribution between Its Inhibitors, Protein C Inhibitor, α1-Antitrypsin and α2-Macroglobulin, in Patients with Disseminated intravascular Coagulation

1993 ◽  
Vol 69 (05) ◽  
pp. 448-453 ◽  
Author(s):  
M F Scully ◽  
C H Toh ◽  
H Hoogendoorn ◽  
R P Manuel ◽  
M E Nesheim ◽  
...  
Keyword(s):  
Western Blotting ◽  
Disseminated Intravascular Coagulation ◽  
Protein C ◽  
Antithrombin Iii ◽  
Clinical Course ◽  
Factor Xa ◽  
Intravascular Coagulation ◽  
Α2 Macroglobulin ◽  
Protein C Inhibitor ◽  
The Face

SummaryActivation and inactivation of protein C during the clinical course of disseminated intravascular coagulation (DIC) was studied in three patients by qualitative (Western blotting) and quantitative (ELISA) analysis and the intensity of procoagulant activity monitored by the measurement of thrombin and factor Xa antithrombin III complexes. In one patient, inhibitor complexes of APC with protein C inhibitor (PCI) and α1-antitrypsin (α1-AT) were observed and the latter predominated at presentation. Both disappeared during the development of remission but the loss of α1-AT complexes preceded PCI complexes which on Western blotting appeared to increase in intensity prior to disappearance. The two other patients bled to death from uncontrollable haemorrhage. In both cases, APC/inhibitor complexes with α2-macroglobulin (α2-M) in addition to PCI and αr-AT were detected and persisted until death. Although PCI appeared to be the primary inhibitor in all three cases, α1-antitrypsin and particularly α2-macroglobulin appeared to assume greater roles in the two fatal cases. These data are similar to previous findings in an experimental animal model of DIC that suggested that α2-macroglobulin and α1-antitrypsin become more important inhibitors of APC as the primary inhibitor PCI is consumed in the face of a sustained procoagulant challenge.

scholarly journals Activation and complexation of protein C and cleavage and decrease of protein S in plasma of patients with intravascular coagulation

Blood ◽  
1989 ◽  
Vol 73 (2) ◽  
pp. 455-461 ◽  
Author(s):  
MJ Heeb ◽  
D Mosher ◽  
JH Griffin
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Protein C ◽  
Activated Protein C ◽  
Protein S ◽  
Coagulation Test ◽  
Major Band ◽  
Intravascular Coagulation ◽  
Protein C Inhibitor ◽  
Dependent Protein

Abstract Activated protein C (APC) is inhibited by two major plasma inhibitors (PCIs). To find evidence for in vivo complexation of APC, immunoblotting studies were performed on plasmas of 85 patients with suspected disseminated intravascular coagulation (DIC). Samples from 62 of these patients contained 5% to 35% of protein C antigen in APC:inhibitor complexes, indicating that protein C activation and inhibition had occurred. In 24 normal plasmas, no detectable APC:PCI complexes were observed (less than 5%). Patients with higher levels of complexes had more abnormal coagulation test data for DIC. The major band of APC complexes detected by anti-protein C antibodies did not react with antibodies to the heparin-dependent protein C inhibitor (PCI- 1) previously described. Rather, APC was complexed with another recently described plasma protein C inhibitor, PCI-2. Immunoblotting studies for protein S, the cofactor for APC, revealed that the majority of the DIC patient plasmas contained a higher than normal proportion of protein S in cleaved form, suggesting that protein S may have been proteolytically inactivated. Protein S total antigen levels were also found to be low in DIC patients, excluding those with malignancy. These studies support the hypothesis that the protein C pathway is activated during DIC.

Effect of Urinary Protein C Inhibitor on Lipopolysaccharide-induced Disseminated Intravascular Coagulation in Rats

2000 ◽  
Vol 84 (07) ◽  
pp. 54-58 ◽  
Author(s):  
Wakako Izutani ◽  
Yoshikazu Komurasaki ◽  
Mitsugu Fujita
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Protein C ◽  
Degradation Products ◽  
Femoral Vein ◽  
Activated Partial Thromboplastin Time ◽  
Urinary Protein ◽  
Fibrinogen Concentration ◽  
Intravascular Coagulation ◽  
Protein C Inhibitor ◽  
Chemotactic Factors

SummaryThe effect of urinary protein C inhibitor (uPCI) on disseminated intravascular coagulation (DIC) was investigated using an experimental DIC in rats. uPCI (0.5 and 1.0 mg/kg) was continuously administrated into the left femoral vein of the rats with lipopolysaccharide (50 mg/kg)-induced DIC. In all doses, uPCI significantly prevented the drastic changes in the parameters such as fibrinogen concentration, activated partial thromboplastin time (APTT), prothrombin time (PT), fibrin/fibrinogen degradation products (FDP) level, aspartate aminotransferase (AST) level and alanine aminotransferase (ALT) level. Furthermore, uPCI significantly inhibited the increase in the levels of plasma kallikrein and thrombin which act not only as the procoagulant proteases but also as the chemotactic factors to neutrophils and monocytes. These results show that uPCI may prevent hypercoagulation, the induction of secondary fibrinolysis and organ failure in the DIC model. Therefore, uPCI may be a useful agent for the clinical treatment of DIC.

scholarly journals Activation and complexation of protein C and cleavage and decrease of protein S in plasma of patients with intravascular coagulation

Blood ◽  
1989 ◽  
Vol 73 (2) ◽  
pp. 455-461
Author(s):  
MJ Heeb ◽  
D Mosher ◽  
JH Griffin
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Protein C ◽  
Activated Protein C ◽  
Protein S ◽  
Coagulation Test ◽  
Major Band ◽  
Intravascular Coagulation ◽  
Protein C Inhibitor ◽  
Dependent Protein

Activated protein C (APC) is inhibited by two major plasma inhibitors (PCIs). To find evidence for in vivo complexation of APC, immunoblotting studies were performed on plasmas of 85 patients with suspected disseminated intravascular coagulation (DIC). Samples from 62 of these patients contained 5% to 35% of protein C antigen in APC:inhibitor complexes, indicating that protein C activation and inhibition had occurred. In 24 normal plasmas, no detectable APC:PCI complexes were observed (less than 5%). Patients with higher levels of complexes had more abnormal coagulation test data for DIC. The major band of APC complexes detected by anti-protein C antibodies did not react with antibodies to the heparin-dependent protein C inhibitor (PCI- 1) previously described. Rather, APC was complexed with another recently described plasma protein C inhibitor, PCI-2. Immunoblotting studies for protein S, the cofactor for APC, revealed that the majority of the DIC patient plasmas contained a higher than normal proportion of protein S in cleaved form, suggesting that protein S may have been proteolytically inactivated. Protein S total antigen levels were also found to be low in DIC patients, excluding those with malignancy. These studies support the hypothesis that the protein C pathway is activated during DIC.

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