scholarly journals A summary of the Japan septic disseminated intravascular coagulation study

2018 ◽  
Vol 5 (2) ◽  
pp. 123-128 ◽  
Author(s):  
Mineji Hayakawa ◽  
Kota Ono
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Intravascular Coagulation ◽  
Coagulation Study

scholarly journals Thrombotic Thrombocytopenic Purpura: Report of a Case With Disseminated Intravascular Platelet Aggregation

Blood ◽  
1973 ◽  
Vol 42 (5) ◽  
pp. 805-814 ◽  
Author(s):  
P. B. Neame ◽  
J. Lechago ◽  
E. T. Ling ◽  
A. Koval
Keyword(s):  
Platelet Aggregation ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Disseminated Intravascular Coagulation ◽  
Endothelial Lining ◽  
Electron Microscopic ◽  
Thrombocytopenic Purpura ◽  
Intravascular Coagulation ◽  
Coagulation Study ◽  
Platelet Aggregates ◽  
Vascular Occlusions

Abstract The nature and etiology of the vascular occlusions encountered in thrombotic thrombocytopenic purpura (TTP) have been subject to controversy for a number of years. Disseminated platelet thrombosis has been suggested in the earlier literature, although later views have favored fibrin thrombi resulting from vascular damage or disseminated intravascular coagulation (DIC). The serial coagulation study and the lightand electron-microscopic findings in a case of TTP are described here. The multiple vascular occlusions were due to the presence of densely packed platelet aggregates in which a variable quantity of fibrin was present. Less commonly, loose platelet aggregates were noted. Fibrin under the endothelial lining was occasionally observed in relationship to the vascular occlusion and was thought to be secondary to the release of various substances from aggregating platelets. The serial coagulation study and the histologic examination of tissues showed no evidence of disseminated intravascular coagulation. This case shows that the occlusions observed in TTP can be due to disseminated intravascular platelet aggregation in the absence of DIC. Although TIP might be of variable etiology, it is felt that cases showing disseminated intravascular platelet aggregation should be distinguished from DIC in order to plan therapy on a rational basis.

Disseminated intravascular coagulation in virus diseases

1967 ◽  
Vol 120 (2) ◽  
pp. 129-152 ◽  
Author(s):  
D. G. McKay
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Virus Diseases ◽  
Intravascular Coagulation

Disseminated intravascular coagulation in meningococcal sepsis

2003 ◽  
Vol 23 (03) ◽  
pp. 125-130 ◽  
Author(s):  
S. Zeerleder ◽  
R. Zürcher Zenklusen ◽  
C. E. Hack ◽  
W. A. Wuillemin
Keyword(s):  
Organ Dysfunction ◽  
Disseminated Intravascular Coagulation ◽  
Skin Necrosis ◽  
Multiple Organ ◽  
Meningococcal Sepsis ◽  
Multiple Organ Dysfunction ◽  
Intravascular Coagulation ◽  
Therapeutic Concepts ◽  
New Therapeutic Concepts ◽  
Coagulation And Fibrinolysis

SummaryWe report on a man (age: 49 years), who died from severe meningococcal sepsis with disseminated intravascular coagulation (DIC), multiple organ dysfunction syndrome and extended skin necrosis. We discuss in detail the pathophysiology of the activation of coagulation and fibrinolysis during sepsis. The article discusses new therapeutic concepts in the treatment of disseminated intravascular coagulation in meningococcal sepsis, too.

Plasma Thrombin Assay using a Chromogenic Substrate in Disseminated Intravascular Coagulation due to Snake Bite Envenomation

1979 ◽  
Vol 41 (03) ◽  
pp. 544-552 ◽  
Author(s):  
R P Herrmann ◽  
P E Bailey
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Degradation Products ◽  
Snake Bite ◽  
Chromogenic Substrate ◽  
Coagulation Parameters ◽  
Fibrinogen Degradation Products ◽  
Intravascular Coagulation

SummaryUsing the chromogenic substrate, Tos-Gly-Pro-Arg-pNA-HCL (Chromozym TH, Boehringer Mannheim) plasma thrombin was estimated in six cases of envenomation by Australian elapid snakes. All patients manifested findings chracteristic of defibrination due to envenomation by these snakes. Fibrin-fibrinogen degradation products were grossly elevated, as was plasma thrombin in all cases.Following treatment with antivenene, all abnormal coagulation parameters returned rapidly towards normal by 24 hours and plasma thrombin disappeared.

The Glycosaminoglycan of Recombinant Human Soluble Thrombomodulin Affects Antithrombotic Activity in a Rat Model of Tissue Factor-Induced Disseminated Intravascular Coagulation

1992 ◽  
Vol 67 (03) ◽  
pp. 366-370 ◽  
Author(s):  
Katsuhiko Nawa ◽  
Teru Itani ◽  
Mayumi Ono ◽  
Katsu-ichi Sakano ◽  
Yasumasa Marumoto ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Disseminated Intravascular Coagulation ◽  
Rat Model ◽  
Chinese Hamster Ovary Cells ◽  
Chinese Hamster ◽  
Soluble Thrombomodulin ◽  
Intravascular Coagulation ◽  
Platelet Counts ◽  
Recombinant Human Soluble Thrombomodulin

SummaryPrevious studies on recombinant human soluble thrombomodulin (rsTM) from Chinese hamster ovary cells revealed that rsTM was expressed as two proteins that differed functionally in vitro due to the presence (rsTMp) or absence (rsTMa) of chondroitin-4-sulfate. The current study evaluates the in vivo behavior of rsTM in rats and in a rat model of tissue factor-induced disseminated intravascular coagulation (DIC). rsTMp was more potent than rsTMa for prolongation of the activated partial thromboplastin time (APTT) and their in vivo half-lives determined by ELISA were 20 min for rsTMp and 5.0 h for rsTMa. Injection of a tissue factor suspension (5 mg/kg) resulted in DIC as judged by decreased platelet counts and fibrinogen concentrations, prolonged APTT, and increased fibrin and fibrinogen degradation products (FDP) levels. A bolus injection of either rsTM (0.2 mg/kg) 1 min before induction of DIC essentially neutralized effects on platelets, fibrinogen, and FDP levels, and had only a moderate effect on APTT prolongation. The dose of anticoagulant to inhibit the drop in platelet counts by 50% (ED50) was 0.2 mg/kg rsTMa, 0.07 mg/kg rsTMp, and 7 U/ kg heparin. The effect of increasing concentrations of rsTM and heparin on bleeding times were compared in experiments involving incision of the rat tail. Doubling of the bleeding times occurred at 5 mg/kg rsTMa, 3 mg/kg rsTMp or 90 U/kg heparin. These values represent a 25-fold increase over the ED50 for rsTMa, 43-fold for rsTMp and 13-fold for heparin. These results suggest that rsTMp is a potent anticoagulant to inhibit the platelet reduction when injected prior to the induction of DIC in rats.

Effect of Anabolic Steroids on Plasma Antithrombin III

1975 ◽  
Vol 34 (01) ◽  
pp. 106-114 ◽  
Author(s):  
I. D Walker ◽  
J. F Davidson ◽  
P Young ◽  
J. A Conkie
Keyword(s):  
Heart Disease ◽  
Ischaemic Heart Disease ◽  
Oral Contraceptives ◽  
Disseminated Intravascular Coagulation ◽  
Fibrinolytic Activity ◽  
Antithrombin Iii ◽  
Anabolic Steroids ◽  
Intravascular Coagulation ◽  
Clear Cut ◽  
Α2 Macroglobulin

SummaryThe effect of seven different anabolic steroids (Ethyloestrenol, Methenolone acetate, Norethandrolone, Methylandrostenediol, Oxymetholone, Methandienone, and Stanozolol) on three α-globulin antiprotease inhibitors of thrombin and plasmin was studied in men with ischaemic heart disease. In distinct contrast to the oral contraceptives, five of the six 17-α-alkylated anabolic steroids studied produced increased plasma Antithrombin III levels and five produced decreased levels of plasma α2-macroglobulin. The effect on plasma α1antitrypsin levels was less clear-cut but three of the steroids examined produced significantly elevated levels. The increased plasma fibrinolytic activity which the 17-α-alkylated anabolic steroids induce is therefore unlikely to be secondary to disseminated intravascular coagulation.

Activation of Hageman Factor by α-Adrenergic Stimulation

1970 ◽  
Vol 23 (03) ◽  
pp. 417-422 ◽  
Author(s):  
D. G McKay ◽  
J.-G Latour ◽  
Mary H. Parrish
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Adrenergic Receptor ◽  
Adrenergic Stimulation ◽  
Hageman Factor ◽  
Intravascular Coagulation ◽  
Receptor Sites ◽  
High Doses ◽  
Stimulation Of

SummaryThe infusion of epinephrine in high doses produces disseminated intravascular coagulation by activation of Hageman factor. The effect is blocked by phenoxybenz-amine and is therefore due to stimulation of α-adrenergic receptor sites.

Increased Tissue Thromboplastin Activity in Monocytes of Patients with Meningococcal Infection: Related to an Unfavourable Prognosis

1983 ◽  
Vol 49 (01) ◽  
pp. 005-007 ◽  
Author(s):  
B Østerud ◽  
T Flægstad
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Fold Increase ◽  
Meningococcal Infection ◽  
High Concentration ◽  
Intravascular Coagulation ◽  
Tissue Thromboplastin ◽  
Unfavourable Prognosis

SummaryIn 16 patients, 13 with meningococcal infection and 3 suspected to have this infection, 8 patients were found to possess significant higher level of tissue thromboplastin activity of their monocytes isolated from the blood at the admission to the hospital than normal. Five of those 8 patients had an extremely high concentration, > 60-300 fold increase, and all these patients died. The exposed tissue thromboplastin activity on the surface of the endotoxin stimulated monocytes is probably the direct inducer of disseminated intravascular coagulation (DIC) in meningococcal infection.

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”.

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