scholarly journals Characterization of fibrinolytic state by measuring crosslinked fibrin degradation products in disseminated intravascular coagulation associated with acute promyelocytic leukemia.

1988 ◽  
Vol 19 (2) ◽  
pp. 217-219
Author(s):  
Kenji OKAJIMA ◽  
Shin KOGA ◽  
Hiroaki OKABE ◽  
Kiyoshi TAKATSUKI
Keyword(s):  
Acute Promyelocytic Leukemia ◽  
Disseminated Intravascular Coagulation ◽  
Degradation Products ◽  
Promyelocytic Leukemia ◽  
Intravascular Coagulation ◽  
Fibrin Degradation Products

Platelet Function in Experimentally Induced Pancreatitis in the Dog

1986 ◽  
Vol 55 (02) ◽  
pp. 197-200 ◽  
Author(s):  
R M Jacobs ◽  
R J Murtaugh ◽  
R H Fertel
Keyword(s):  
Platelet Function ◽  
Disseminated Intravascular Coagulation ◽  
Degradation Products ◽  
Plasma Concentrations ◽  
Adenosine Diphosphate ◽  
Intravascular Coagulation ◽  
Fibrin Degradation Products ◽  
Functional Defect ◽  
And Function ◽  
Experimentally Induced

SummaryEvidence suggests that changes in prostaglandins and disseminated intravascular coagulation accompany pancreatitis. Both may induce changes in platelet function. We wished to determine if experimentally induced pancreatitis in the dog was associated with altered platelet number and function, and whether there were concomitant changes in prostaglandins. Evidence for disseminated intravascular coagulation in the dogs with pancreatitis were red blood cell fragmentation, increased platelet turnover indicated by macro-platelets and the transient presence of fibrin degradation products in urine. There were no significant changes in platelet count. The platelets from dogs with pancreatitis showed a functional defect characterized by significantly decreased aggregation in response to adenosine diphosphate, arachidonic acid, and collagen. Release of adenosine triphosphate from platelets was reduced in collagen-stimulated aggregation. There were no changes in the plasma concentrations of thromboxane B2, 6-Keto-PGF1a, and PGE2. This defect may have been due to the generation of fibrin degradation products and platelet “exhaustion”.

scholarly journals Acute Promyelocytic Leukemia: Results of Treatment by Daunorubicin

Blood ◽  
1973 ◽  
Vol 41 (4) ◽  
pp. 489-496 ◽  
Author(s):  
Jean Bernard ◽  
Marise Weil ◽  
Michel Boiron ◽  
Claude Jacquillat ◽  
Georges Flandrin ◽  
...  
Keyword(s):  
Acute Promyelocytic Leukemia ◽  
Median Duration ◽  
Disseminated Intravascular Coagulation ◽  
Promyelocytic Leukemia ◽  
The Other ◽  
Intravascular Coagulation ◽  
Results Of Treatment

Abstract Daunorubicin induces complete remissions in about 50% of patients with acute promyelocytic leukemia. The median duration of these remission is 26 mo. Failures are mainly due to hemorrhages as a result of disseminated intravascular coagulation during the first 5 days (25%) or due to sepsis during the second and third week (25%). Long-term survivals are more frequent than in the other acute granulocytic leukemias.

scholarly journals D-dimer kit with a High FDP/D-Dimer Ratio is Useful for Diagnosing Thrombotic Diseases

2022 ◽  
Vol 28 ◽  
pp. 107602962110705
Author(s):  
Nozomi Ikeda ◽  
Hideo Wada ◽  
Yuhuko Ichikawa ◽  
Minoru Ezaki ◽  
Motoko Tanaka ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Critically Ill ◽  
Disseminated Intravascular Coagulation ◽  
Critically Ill Patients ◽  
Degradation Products ◽  
Intravascular Coagulation ◽  
Fibrin Degradation Products ◽  
Peripheral Arterial ◽  
Thrombotic Diseases ◽  
D Dimer

Introduction Although D-dimer is a useful biomarker of thrombosis, there are many D-dimer kits, with high and low fibrinogen and fibrin degradation products (FDP)/ D-dimer ratios. Methods Plasma D-dimer levels were measured using three different kits in critically ill patients to examine the usefulness of such measurements for detecting the thrombotic diseases and determining the correlation with the FDP and FDP/D-dimer ratio. Results Although three D-dimer kits showed marked utility for diagnosing disseminated intravascular coagulation (DIC) and peripheral arterial and venous thromboembolism (PAVTE), the D-dimer levels determined using the three kits varied among diseases. Indeed, one D-dimer kit showed a high FDP/D-dimer ratio, and another kit showed a low FDP/D-dimer ratio. D-dimer kit with low FDP/D-dimer ratio tended to have high cut-off values and low specificity for diagnosing DIC and PAVTE. In D-dimer kit with high FDP/D-dimer ratio, FDP/D-dimer ratios in patients with thrombosis was significantly higher than that in patients without thrombosis. Conclusion All three D-dimer kits show utility for detecting thrombotic diseases. However, the D-dimer levels determined using the kits varied due to differences in the FDP/D-dimer ratio. In combination with the FDP level, a D-dimer kit with a high FDP/D-dimer ratio may be useful.

scholarly journals The specific activity of plasminogen activator inhibitor-1 in disseminated intravascular coagulation with acute promyelocytic leukemia

Blood ◽  
1991 ◽  
Vol 77 (9) ◽  
pp. 1949-1957 ◽  
Author(s):  
Y Sakata ◽  
T Murakami ◽  
A Noro ◽  
K Mori ◽  
M Matsuda
Keyword(s):  
Plasminogen Activator ◽  
Acute Promyelocytic Leukemia ◽  
Disseminated Intravascular Coagulation ◽  
Specific Activity ◽  
Plasminogen Activator Inhibitor ◽  
Promyelocytic Leukemia ◽  
Plasminogen Activator Inhibitor 1 ◽  
Intravascular Coagulation ◽  
Activator Inhibitor ◽  
Pai 1

In disseminated intravascular coagulation (DIC) with acute promyelocytic leukemia (APL) in the absence of severe infection, marked fibrinolysis was noted in comparison with normal levels of antithrombin III, which is a major inhibitor of the coagulation system. Increased plasminogen activator inhibitor-1 (PAI-1) antigen levels in plasma from patients with septicemia decreased the ratio of the plasma clot lysis rate induced by an anti-alpha 2-plasmin inhibitor monoclonal antibody to the tissue-type plasminogen activator (t-PA) concentration. This decrease was not as prominent in plasma from patients with DIC, especially those with APL. To explore the character of PAI-1 in these plasmas, we measured the specific activity of PAI-1 by determining the ratio of active PAI-1 antigen to t-PA-unbound PAI-1 antigen. To calculate the amount of active PAI-1 antigen, the amount of t-PA/PAI-1 complex before and after the addition of a fixed amount of t-PA to the sample was measured by a sandwich solid-phase enzyme-linked immunosorbent assay using anti-PAI-1 and anti-t-PA monoclonal antibodies. The assay to measure total PAI-1 antigen used three monoclonal anti-PAI-1 antibodies and had similar sensitivities to free active, latent, vitronectin-bound and t-PA-bound PAI-1. The specific activity of PAI-1 decreased in patients with DIC (43.7% +/- 30.6%) and in DIC cases with APL (10.3% +/- 6.0%) in comparison to patients with septicemia (83.7% +/- 20.2%) or normal controls (85.8% +/- 27.3%). In DIC associated with APL, degraded forms of PAI-1 were detected in plasma by immunoblotting. These results suggest that a decrease in the specific activity of PAI-1 and an increase in secondary fibrinolysis result in a hyperfibrinolytic state in DIC patients with APL.

Sign in / Sign up

Export Citation Format

Share Document