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

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.

1989 ◽  
Vol 35 (9) ◽  
pp. 1897-1900 ◽  
Author(s):  
C Fukuda ◽  
K Iijima ◽  
K Nakamura

Abstract This is a method for measuring tissue factor (TF, Factor III, tissue thromboplastin) activity in plasma by using a chromogenic substrate. As pretreatment, the euglobulin fraction of plasma was prepared by removing endogenous inhibitors and heated at 60 degrees C for 3 min to remove fibrinogen. This allowed us to measure the low TF activity in plasma that could not otherwise be measured. Neither phospholipids nor coagulation factors VII, IX, X, or Xa in the samples interfere. Within-run and day-to-day reproducibility were both good. The mean value obtained by this method for normal persons was 1.02 (SD 0.91) arbitrary units/L. A markedly high plasma TF activity of 20 arb. units/L or more was observed in patients with some types of disseminated intravascular coagulation.


1973 ◽  
Vol 30 (01) ◽  
pp. 025-035 ◽  
Author(s):  
Fredrik Skjørten ◽  
Stein A. Evensen

SummaryBirds are naturally deficient in the coagulation factors responsible for the contact activation reactions in mammalian plasma. In the present study, fowl lungs were examined for evidence of disseminated intravascular coagulation (DIC) 5 min or 4 hours after injection of either Liquoid or bacterial endotoxin. These substances are potent initiators of DIC in mammals, and activation of factor XII is believed to be essential for their triggering effect.Liquoid injection produced intravascular deposits with the light microscopical staining properties of fibrin. However these deposits had a purely granular ultra-structure; their formation was not prevented by adequate anticoagulation, and there was no concomitant thrombocyte aggregation. It is suggested that the deposits represent precipitates of plasma proteins, including fibrinogen.Endotoxin failed to produce clinical reactions, intravascular deposits or thrombocyte aggregates. In contrast, animals injected with homologous tissue thromboplastin died, and fibrillar material with the ultrastructural appearance of fibrin, as well as thrombocyte aggregates were found in small pulmonary vessels. These effects were completely prevented by anticoagulation.We conclude that both Liquoid and endotoxin failed to trigger DIC in the factor XII-deficient fowl, suggesting that these substances depend on the contact activation reactions for the generation of thrombin.


1975 ◽  
Author(s):  
N. Sakuragawa ◽  
K. Takahashi ◽  
M. Matsuoka

Prothrombin is decreased in disseminated intravascular coagulation syndrome (DIC). Prothrombin is estimated by the assay method using echis carinatus venom: 0.1 ml of 0.1% fibrinogen solution, 0.1 ml of one to ten diluted specimen and 0.1 ml of echis carinatus venom solution (0.01 mg/ml) are mixed in the test tube at 37° 0, and checked clotting time. From the standard calibration curve, prothrombin is shown by percentage in a normal person.Prothrombin activity by the regular assay method using tissue thromboplastin is lower than the assay method using echis carinatus venom in DIC.Thrombin which is produced in the blood of DIC splits prothrombin molecule to prethrombin. Prothrombin cannot be assayed by using tissue thromboplastin, but assayed rather by echis carinatus venom. This fact is proven from the results of SDS-dise electropboresis”pattern of purified prothrombin activated by thrombin or echis carinatus venom, by animal studies of DIC rabbit infused with thrombin, and by examination of DIC blood.‘ The assay method using echis carinatus venom is concluded to be useful to diagnose DIC.


1981 ◽  
Vol 54 (2) ◽  
pp. 264-267 ◽  
Author(s):  
Susan Shurin ◽  
Harold Rekate

✓ A child who developed generalized bleeding immediately after placement of a ventriculoperitoneal shunt was found to have evidence of disseminated intravascular coagulation (DIC). Infusion of fresh frozen plasma was followed promptly by improvement in laboratory values and cessation of bleeding. Complications of the acute bleeding episode included intraventricular hemorrhage, loss of 50% of the red cell volume into subcutaneous tissues, and transient peritoneal irritation. Defibrination syndrome (that is, DIC) due to release of tissue thromboplastin is a recognized complication of trauma, particularly with brain injury. Defibrination can be induced in experimental systems with administration of very small amounts of thromboplastin, which is present in high concentration in brain tissue. This has not been described previously with minor neurosurgical procedures. The diagnosis of DIC should be considered if excessive bleeding occurs after any brain insult, since early recognition and restoration of normal hemostasis by replacement of clotting factors should prevent major complications due to ongoing hemorrhage.


1994 ◽  
Vol 76 (4) ◽  
pp. 353-362 ◽  
Author(s):  
Yasuhiro. Katsuura ◽  
Kumiko. Aoki ◽  
Hirofumi. Tanabe ◽  
Mamoru. Kiyoki ◽  
Akinobu. Funatsu

2019 ◽  
Vol 25 ◽  
pp. 107602961984333 ◽  
Author(s):  
Priya Patel ◽  
Amanda Walborn ◽  
Matthew Rondina ◽  
Jawed Fareed ◽  
Debra Hoppensteadt

Sepsis is a severe systemic inflammatory response to infection that manifests with widespread inflammation as well as endothelial and coagulation dysfunction that may lead to hypotension, organ failure, shock, and death. Disseminated intravascular coagulation (DIC) is a complication of sepsis involving systemic activation of the fibrinolytic and coagulation pathways that can lead to multi-organ dysfunction, thrombosis, and bleeding, with a 2-fold increase in mortality. This study demonstrates the diagnostic and prognostic value of profiling various biomarkers of inflammation and infection in patients with sepsis-associated DIC to assess the severity of illness. Deidentified samples were obtained from adult patients with sepsis and suspected DIC. Platelet count, prothrombin time, D-dimer, and fibrinogen levels were used to assign International Society of Thrombosis and Hemostasis DIC scores to plasma samples from 103 patients with sepsis and suspected DIC. Using commercially available enzyme-linked immunosorbent assay, chromogenic assay, and RANDOX Biochip methods, levels of procalcitonin (PCT), extracellular nucleosomes, interleukin (IL) 6, IL-8, IL-10, and tumor necrosis factor α (TNFα) were measured in patients with sepsis and DIC and compared to levels in healthy individuals. Elevated levels of PCT, IL-6, IL-8, IL-10, and TNFα were observed in most patients with sepsis and DIC. Additionally, the levels of these markers show significant positive correlations with each other and with DIC score. Currently, no single biomarker can effectively diagnose DIC in patients with sepsis. This study lays the groundwork for the development of a diagnostic algorithm using several markers of inflammation and infection and DIC score as parameters in assessing severity of sepsis-associated coagulopathy in a clinical setting.


1987 ◽  
Vol 57 (02) ◽  
pp. 165-170 ◽  
Author(s):  
H Hara ◽  
Y Tamao ◽  
R Kikumoto ◽  
S Okamoto

SummaryWe examined the effect of a synthetic thrombin inhibitor, MCI-9038, on two experimental animal models of disseminated intravascular coagulation (DIC).In a model that DIC induced by the intravenous infusion of thrombin, MCI-9038 suppressed the decrease of platelet count by about 50% at a dose of 0.2 μg/kg/min and almost completely at 2 μg/kg/min. When MCI-9038 was administered orally, the suppressive effect was also observed. Heparin suppressed the platelet count decrease by about 50% at 1 unit/kg/min.In another model of DIC induced by lactic acid and tissue thromboplastin infusion, MCI-9038 prevented the decrease of platelet count and the consumption of coagulation factors. The suppression effect by about 50% on these changes was observed at a dose of 3.16 μg/kg/min. Thromboelastogram pattern indicating the consumption coagulopathy in control experiments was normalized by the MCI-9038 administration. Heparin suppressed the decrease of fibrinogen content as effectively as MCI-9038, but it was less effective on the platelet count decrease.From these results, it was concluded that MCI-9038 might be useful for the treatment of DIC.


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