Causes of a Negative Ethanol Gelation Test in Diffuse Intravascular Coagulation

1974 ◽  
Vol 31 (02) ◽  
pp. 299-308 ◽  
Author(s):  
W. B. J Gerrits ◽  
Elisabeth M Prakke ◽  
J van der Meer ◽  
J Vreeken
Keyword(s):  
Fibrinogen Level ◽  
Degradation Products ◽  
Laboratory Data ◽  
Aminocaproic Acid ◽  
Plasmin Activity ◽  
Clinical Value ◽  
Intravascular Coagulation ◽  
Diffuse Intravascular Coagulation ◽  
Gelation Test

SummaryThe clinical value of the ethanol gelation test (EGT) in diagnosing diffuse intravascular coagulation (DIC) has been questioned because of the occasional finding of a negative test, while other laboratory data pointed to DIC. Therefore, the behaviour of the EGT during thrombin infusions in rabbits was studied, with special reference to the fibrinogen level and activation of fibrinolysis. Fibrinolytic activity was inhibited or induced by synchronous infusion of epsilon-aminocaproic acid or plasmin respectively. The results obtained show that apart from severe depletion of fibrinogen strong activation of fibrinolysis can cause a negative EGT during thrombin infusions in rabbits. This phenomenon could not be ascribed to high levels of fibrin degradation products (fdp); it might be due to plasmin digestion of fibrin monomers. In vitro studies with human plasma confirmed that the EGT becomes negative at a fibrinogen level of less than 20 mg per 100 ml or by plasmin activity in the presence of a normal fibrinogen level.Whereas a positive EGT is highly specific for DIC, these studies show that a negative EGT does not exclude the presence of DIC.

Disseminated Intravascular Coagulation: A Clinical/Laboratory Correlation In 48 Patients

1981 ◽  
Author(s):  
R L Bick
Keyword(s):  
Platelet Count ◽  
Disseminated Intravascular Coagulation ◽  
Clinical Laboratory ◽  
Fibrinogen Level ◽  
Degradation Products ◽  
Severe Bleeding ◽  
Thrombin Time ◽  
Intravascular Coagulation ◽  
At Iii ◽  
Pre Treatment

Disseminated intravascular coagulation (DIC) is a frequent clinical entity spanning from a moderately severe bleeding disorder to a catastrophic, fulminant, and often fatal form usually associated with hemorrhage or, less commonly,as diffuse thromboses. The clinical and laboratory features of DIC remain confusing and controversial. To critically evaluate the usefulness of coagulation tests in aiding in the diagnosis and monitoring of therapy in DIC the clinical and laboratory findings were summarized in 48 patients with DIC. All patients were subjected to a prothrombin time (PT), activated partial thromboplastin time (PTT), reptilase time (RT), thrombin time (TT), fibrin(ogen) degradation products (FDP), platelet count, protamine sulfate test (PSO4), fibrinogen determination, and biological antithrombin-III (AT-III) level at the time of diagnosis. In addition, these same laboratory modalities were used to monitor patients during and after therapy. In this series of 48 patients, 38 patients had acute DIC and 10 patients had chronic DIC. In those patients with acute DIC, 100% of patients presented with hemorrhage and 53% of patients had thrombosis; 26% of patients died of their DIC type syndrome. In those patients with chronic DIC, 100% presented with hemorrhage, 80% presented with thrombosis, and none died of their intravascular clotting process. The probability of a pre-treatment abnormality in acute DIC was: FDP > AT-III = platelet count PS04 > TT > PT > fibrinogen level > PTT > RT. The probability of pre-treatment abnormalties in chronic DIC was: FDP > PSO4 = PT > AT-III = RT platelet count fibrinogen level = TT. These studies suggest the FDP level, the AT-III level, PSO4, and fibrinogen level to be reliable for aiding in the diagnosis of acute DIC. In chronic DIC the fibrinogen level, PS04, PTT, and AT-III level appear to be the most reliable indicies.

Effect of Vitamin E on Endotoxin-Induced Disseminated Intravascular Coagulation in Rats

1982 ◽  
Vol 48 (02) ◽  
pp. 235-237 ◽  
Author(s):  
T Yoshikawa ◽  
Y Furukawa ◽  
M Murakami ◽  
K Watanabe ◽  
M Kondo
Keyword(s):  
Platelet Count ◽  
Vitamin E ◽  
Disseminated Intravascular Coagulation ◽  
Fibrinogen Level ◽  
Degradation Products ◽  
Tocopheryl Acetate ◽  
Preventive Effect ◽  
Intravascular Coagulation ◽  
Fibrin Degradation Products ◽  
Fibrin Thrombi

SummaryExperimental disseminated intravascular coagulation (DIC) can be induced by 4 hr sustained infusion of endotoxin in a dose of 100 mg/kg in rats. The experimental model of DIC in rats was used to study the preventive effect of vitamin E, α-tocopheryl acetate, against DIC. Before the infusion of endotoxin, 0.01, 0.1, 1.0 or 10.0 mg/kg/day of α-tocopheryl acetate was injected intraperitoneally for 4 successive days. The preventive effect against DIC was noted in all the parameters, such as fibrinogen and fibrin degradation products, fibrinogen level, prothrombin time, partial thromboplastin time, platelet count, and the number of renal glomeruli with fibrin thrombi, in rats treated with 1.0 or 10.0 mg/kg of α-tocopheryl acetate. From these results, it was shown that vitamin E, α-tocopheryl acetate, inhibited endotoxin-induced experimental DIC in rats.

Effects of Ticlopidine and Aspirin on Endotoxin-Induced Disseminated Intravascular Coagulation in Rats

1983 ◽  
Vol 49 (03) ◽  
pp. 190-192 ◽  
Author(s):  
T Yoshikawa ◽  
M Murakami ◽  
Y Furukawa ◽  
S Takemura ◽  
M Kondo
Keyword(s):  
Platelet Count ◽  
Continuous Infusion ◽  
Disseminated Intravascular Coagulation ◽  
Partial Thromboplastin Time ◽  
Fibrinogen Level ◽  
Degradation Products ◽  
Preventive Effect ◽  
Intravascular Coagulation ◽  
Fibrin Degradation Products ◽  
Fibrin Thrombi

SummaryThe effects of ticlopidine and aspirin on endotoxin-induced experimental disseminated intravascular coagulation (DIC) were studied in rats. Experimental DIC was induced by a 4 hr sustained infusion of endotoxin at a dose of 100 mg/kg. The rats were intraperitoneally injected with ticlopidine at 2.0, 20.0, 50.0, 100.0 or 200.0 mg/kg, or aspirin at 0.03, 0.3, 3.0 or 30.0 mg/kg, followed by the continuous infusion of 100 mg/kg/4 hr of endotoxin. A preventive effect against DIC was noted in all the parameters, such as fibrinogen and fibrin degradation products (FDP), fibrinogen level, prothrombin time, partial thromboplastin time (PTT), platelet count and the number of renal glomeruli with fibrin thrombi, in the rats treated with 20.0, 50.0, 100.0 or mg/kg of ticlopidine. Although a preventive effect was also noted in FDP, PTT, platelet count and the number of glomeruli with thrombi in rats treated with 0.03 or 0.3 mg/kg of aspirin, this agent was less effective than ticlopidine.

Mafenide (Sulfamylon™) Inhibits Plasmin Fibrinolytic Activity

1988 ◽  
Vol 59 (03) ◽  
pp. 440-444 ◽  
Author(s):  
Daniel J Weisdorf ◽  
Jeffrey H Aldridge
Keyword(s):  
Skin Graft ◽  
Binding Sites ◽  
Fibrinolytic Activity ◽  
Aminocaproic Acid ◽  
Acetate Solution ◽  
Plasmin Activity ◽  
Burn Wounds ◽  
Fibrinolytic Potential ◽  
Topical Antimicrobial

SummaryInflammatory fibrinolysis by plasmin or phagocyte proteases is a major cause of skin graft failure on burn wounds where the primary adherent attachment of the skin grafts is due to the gluelike action of fibrin. We investigated the potential of mafenide acetate solution, an experimental topical antimicrobial used in treating grafted burn wounds, to modify plasmin fibrinolytic activity in vitro and, thus, its potential to alter or modify the integrity of the fibrin glue critical for skin graft viability. Immobilized 125I-fibrin monolayers were used to assay fibrinolytic activity from plasmin or from plasma activated by streptokinase or urokinase and modified by the presence of mafenide or ε-aminocaproic acid (EACA). While streptokinase-activated plasma lysed 52.7 ± 3.9% of the 125I-fibrin, this plasmin activity was more than 80% inhibitable by EACA. Mafenide acetate had no intrinsic fibrinolytic activity (1.5 ± 0.3%) nor activated plasma fibrinolytic potential (2.4 ± 0.5%), but produced significant and dose-related reduction in fibrinolytic activity (p <0.001). Other sulfonamide analogues lacking a para-methylamino reactive group had 10–100 fold less antifibrinolytic potency while lysine, like mafenide, able to compete for plasmin binding sites, could potently block fibrinolysis. Mafenide did not qualitatively alter activation of plasminogen or affect generation of complexes with α2 antiplasmin complexes. Adding mafenide only minutes following streptokinase-activated plasma or plasmin with the fibrin substrate reduced antifibrinolytic activity, supporting the conclusion that mafenide, like EACA, can modulate the interaction between fibrin and the plasmin reactive sites and thus prevent close plasmin/fibrin apposition. The union of mafenide’s potent antimicrobial activity with its antifibrinolytic potential is a fortuitous combination. The beneficial antifibrinolytic effect of mafenide may control inflammatory proteolysis, promote skin graft retention, and support wound healing.

A Comparative Study of Human and Monkey (Macaca irus) Fibrinogen Degradation Products

1974 ◽  
Vol 31 (02) ◽  
pp. 319-327
Author(s):  
Thomas R Poskitt ◽  
H Philip Fortwengler ◽  
Gerald J Roth ◽  
James A Eaton
Keyword(s):  
Comparative Study ◽  
Disseminated Intravascular Coagulation ◽  
Degradation Products ◽  
Gel Filtration ◽  
Fibrinogen Degradation Products ◽  
Pathogenic Mechanisms ◽  
Intravascular Coagulation ◽  
High Degree ◽  
Degree Of Similarity

SummaryImmunochemical, physical, and anticoagulant properties of human and monkey (Macaca irus) fibrinogen degradation products (FDP’s) were compared by Immunoelectrophoresis, Sephadex G-200 gel filtration, and anticoagulant assay. Both species demonstrated a high degree of similarity in the properties and sequence of generation of FDP’s derived from in vitro plasmin digestion of highly purified fibrinogen. The results of this study should permit a closer analogy to be drawn between the pathogenic mechanisms of disseminated intravascular coagulation occurring experimentally in monkeys and clinically in humans.

Comparison of Ethanol and Protamine Tests in Demonstration of Soluble Fibrin and Early Products of Fibrin Degradation

1972 ◽  
Vol 28 (03) ◽  
pp. 342-350 ◽  
Author(s):  
Y. P Konttinen ◽  
L Kemppainen ◽  
O Turunen
Keyword(s):  
Spectrophotometric Method ◽  
Degradation Products ◽  
The Other ◽  
Clot Lysis ◽  
Fibrinogen Degradation Products ◽  
Soluble Fibrin ◽  
Intravascular Coagulation ◽  
Fibrin Monomer ◽  
Other Hand ◽  
Gelation Test

SummaryPerformance and applicability of ethanol-induced gelation and protamine-induced paracoagulation for the demonstration of soluble fibrin monomer complexes and fragment Xo complexes was studied by using 1. fibrin monomer plasma prepared by adding small amounts of thrombin to plasma, 2. clot lysis products, and 3. thrombin -treated mixture of fibrinogen degradation products and plasma. To increase the specificity of the protamine tests only visible fibrin strand formation was recorded as positive. In addition to qualitative tests the amount of paracoagulable material was measured by a spectrophotometric method.The ethanol gelation test proved very simple, reproducible and considerably more sensitive than the protamine tests in demonstrating soluble fibrin monomer complexes, irrespective of whether fibrinogen degradation products were present or not. On the other hand, the protamine tests were clearly superior for demonstration of clot lysis products (fragment Xo complexes). Therefore it seems advisable to perform both types of tests when screening for intravascular coagulation.

Effects of Superoxide Dismutase and Catalase on Disseminated Intravascular Coagulation In Rats

1983 ◽  
Vol 50 (04) ◽  
pp. 869-872 ◽  
Author(s):  
T Yoshikawa ◽  
M Murakami ◽  
N Yoshida ◽  
O Seto ◽  
M Kondo
Keyword(s):  
Superoxide Dismutase ◽  
Platelet Count ◽  
Disseminated Intravascular Coagulation ◽  
Fibrinogen Level ◽  
Degradation Products ◽  
Preventive Effect ◽  
Endotoxin Infusion ◽  
Intravascular Coagulation ◽  
Fibrin Degradation Products ◽  
Fibrin Thrombi

SummaryThe effects of superoxide dismutase (SOD) and catalase on endotoxin-induced experimental disseminated intravascular coagulation (DIC) were studied in rats. Experimental DIC was induced by a 4 hr sustained infusion of endotoxin at a dose of 100 mg/kg. The rats were subcutaneously injected with SOD at 0.5, 5.0 or 50.0 mg/kg, or catalase at 0.01, 0.1 or 1.0 mg/kg, followed by the continuously infusion of 100 mg/kg/4hr of endotoxin. A preventive effect against DIC was noted in all the parameters, such as fibrinogen and fibrin degradation products, fibrinogen level, prothrombin time, partial thromboplastin time, platelet count and the number of renal glomeruli with fibrin thrombi, in the rats treated with 50.0 mg/kg of SOD or 1.0 mg/kg of catalase. When 50.0 mg/kg of SOD or 1.0 mg/kg of catalse was injected subcutaneously at 1, 2 or 3 hr after the initiation of the endotoxin-infusion, the protective effect against DIC was noted in all the parameters.

Fibrinogen Consumption In Breast Cancer And Its Relation To The Extent And Type Of Metastases

1981 ◽  
Author(s):  
V Pengo ◽  
G Cartei ◽  
D Casara ◽  
C Guerra ◽  
E Bertaglia ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Patients ◽  
Half Life ◽  
Fibrinogen Level ◽  
Degradation Products ◽  
Breast Cancer Patients ◽  
Normal Range ◽  
Fibrin Degradation Products ◽  
Extent Of Disease ◽  
Gelation Test

A subclinical intravascular coagulation-fibrinolysis syndrome (I.C.F.), is commonly present in cancer patients: a shortened fibrinogen halflife, in fact, have been found in most patients with malignancies, not considering, however, the type and extent of disease. 28 breast cancer patients, without bleeding and thromboembolic disorders and not receiving chemo-radiotherapy, have been assessed for the presence of I.C.F. syndrome by mean of radiofibrinogen half-life, fibrinogen level, ethanol gelation test, fibri- nogen/fibrin degradation products (FDP). 16 patients without metastases were studied before surgery, while 12 patients with metastases were studied after more than one month from the operation (7 diffuse metastases, 5 pulmonar metastases). 14 out of 16 patients of the first group, and 6 out of 7 with diffuse metastases showed a markedly shortened fibrinogen half-life (hours) (x=53.9±18.2, x=54.2±16.4 as mean±SD respectively), while all the patients with pulmonar metastases showed a normal fibrinogen half-life (x=84±9.9). Normal range was 73-91 h. FDP were almost always normal. In conclusion the tumor per se determine a fibrinogen consumption without a competent fibrinolysis. Pulmonar metastases don’t promote fibrinogen consumption and/or they don’t need fibrin for their growth and spread,

A Novel Platelet Activating Factor Antagonist, SM-12502, Attenuates Endotoxin-induced Disseminated Intravascular Coagulation and Acute Pulmonary Vascular Injury by Inhibiting TNF Production in Rats

1996 ◽  
Vol 75 (06) ◽  
pp. 965-970 ◽  
Author(s):  
Kazunori Murakami ◽  
Kenji Okajima ◽  
Mitsuhiro Uchiba ◽  
Masayoshi Johno ◽  
Hiroaki Okabe ◽  
...  
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Degradation Products ◽  
Platelet Activating Factor ◽  
Pulmonary Vascular Permeability ◽  
Intravascular Coagulation ◽  
Tnf Α ◽  
Histologic Changes ◽  
Factor Antagonist

SummaryAdult respiratory distress syndrome and disseminated intravascular coagulation are important pathologic conditions affecting the outcome of patients with sepsis. To elucidate the possible therapeutic efficacy of SM-12502, a novel platelet activating factor antagonist, on acute lung injury and disseminated intravascular coagulation in sepsis, we investigated the effect of SM-12502 on an endotoxin (ET)-induced septic model in rats. SM-12502 prevented ET-induced increases in pulmonary vascular permeability and ET-induced histologic changes, such as leukocyte infiltration and pulmonary interstitial edema, 6 h following the administration of ET (5 mg/kg). SM-12502 also inhibited the decrease in fibrinogen and the increase in fibrin and fibrinogen degradation products observed following ET administration. SM-12502 prevented increases in the serum concentration of tumor necrosis factor (TNF) 90 min following ET administration in vivo, and significantly inhibited the production of TNF-α by ET-stimulated monocytes in vitro.These findings suggest that SM-12502 attenuates the actions of endotoxin by the inhibition of TNF production

Quantitation of the Coagulation Inhibition in Vivo Due to Breakdown Products of Fibrin

1970 ◽  
Vol 23 (03) ◽  
pp. 477-485 ◽  
Author(s):  
P. S Mitchell ◽  
F. K Beller
Keyword(s):  
Blood Clotting ◽  
Fibrinogen Level ◽  
Degradation Products ◽  
Thrombin Time ◽  
Clotting Time ◽  
Human Fibrinogen ◽  
Quantitative Basis ◽  
Coagulation Inhibition

SummaryDegradation products of human fibrinogen were prepared by in vitro lysis of fibrin clots by urokinase activation and injected into rabbits on a quantitative basis. The dose necessary to anticoagulate the animal was equal to 2½ to 3 times the animals’ fibrinogen level. The effect on whole blood clotting time and thrombin time lasted for approximately 2 hrs. The “r” time of the TEG returned to normal after 1 hr while the “Max” value remained abnormal for more than 120 min. Degradation product E was shown to clear more rapidly than D by immunochemical techniques. The overall T ½ clearance was found to be approximately 12 hrs.

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