Kinetics Of Antithrombin III During Severe Consumption Coagulopathy In An Infant Measured Without Radioactive Tracer Proteins

1981 ◽  
Author(s):  
B Schmidt ◽  
U Wais ◽  
I Witt ◽  
W Pringsheim ◽  
W Künz
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Antithrombin Iii ◽  
Radioactive Tracer ◽  
Coagulation Factors ◽  
Turnover Rates ◽  
Intravascular Coagulation ◽  
Elimination Half ◽  
Coagulation Proteins ◽  
Precise Diagnosis ◽  
Severe Coagulopathy

The precise diagnosis of disseminated intravascular coagulation remains difficult to achieve: Decreased production of coagulation factors and/or thrombocytes can mimic the laboratory pattern of disseminated intravascular coagulation. The measurement of increased turnover rates for coagulation proteins would provide more convincing criteria.During the course of severe coagulopathy in an infant suffering from septicaemia and shock, antithrombin levels were determined repeatedly before and during treatment with Antithrombin concentrate: Activities and concentrations were measured, using chromogenic substrates and immunodiffusion plates, respectively. By mathematical analysis of these data, using a biexponential function, the plasma elimination half-life of the antithrombin III was estimated to be 7.5 to 10.5 hours. Compared with known plasma half-lives of radioactively labelled antithrombin III in adults, the increase was five- to ten-fold. This indicates an accelerated consumption of antithrombin III in this case of severe coagulopathy.

Disseminated Intravascular Coagulation in Cancer: An Update

2019 ◽  
Vol 45 (04) ◽  
pp. 342-347 ◽  
Author(s):  
Marcel Levi
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Inflammatory Responses ◽  
Traumatic Injury ◽  
Distant Metastases ◽  
Coagulation Factors ◽  
Bleeding Complications ◽  
Adequate Treatment ◽  
Intravascular Coagulation ◽  
Coagulation Proteins ◽  
Thrombotic Complications

AbstractCancer often leads to the activation of coagulation, manifesting as disseminated intravascular coagulation (DIC) in its most extreme form. DIC is characterized by systemic intravascular coagulation activation (leading to deposition of intravascular platelets and fibrin) and simultaneous consumption of coagulation proteins and thrombocytes (which may cause bleeding complications). The clinical course of DIC in patients with malignancies is typically less intense compared with DIC complicating alternative clinical settings, including systemic inflammatory responses following infection or traumatic injury. A more slowly proceeding, less fulminant, and widespread hemostatic derangement can remain asymptomatic. Eventually, the ongoing consumption may result in low levels of platelets and coagulation factors, and bleeding complications (frequently localized at the site of the tumor or distant metastases) may be the first clinical manifestation of DIC. An alternative clinical scenario is dominated by thrombotic complications, ranging from clinically manifest vascular thrombosis to microvascular platelet plugs. The main principle of DIC management is adequate treatment of the precipitating disorder; however, there are clinical presentations that may require additional supportive strategies specifically aimed at the amelioration of the coagulopathy.

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.

Successful Evacuation of Subdural Hematoma in the Presence of Severe Coagulopathy

Neurosurgery ◽  
1982 ◽  
Vol 11 (2) ◽  
pp. 277-279 ◽  
Author(s):  
Ken Winston ◽  
Scott Conner
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Satisfactory Result ◽  
Subdural Hematoma ◽  
Acute Subdural Hematoma ◽  
Intravascular Coagulation ◽  
Severe Coagulopathy

Abstract An acute subdural hematoma was evacuated in the presence of a severe coagulopathy that was probably due to disseminated intravascular coagulation. A satisfactory result was achieved.

Antithrombin III (AT-III) as a diagnostic aid in disseminated intravascular coagulation

1977 ◽  
Vol 10 (5) ◽  
pp. 721-729 ◽  
Author(s):  
Rodger L. Bick ◽  
Mildred L. Dukes ◽  
William L. Wilson ◽  
Lajos F. Fekete
Keyword(s):  
Disseminated Intravascular Coagulation ◽  
Antithrombin Iii ◽  
Diagnostic Aid ◽  
Intravascular Coagulation ◽  
At Iii

scholarly journals Simvastatin improves the prognosis of endotoxin-induced disseminated intravascular coagulation by regulating the intestinal microenvironment

2020 ◽  
Author(s):  
Min Xu ◽  
Lili Luo ◽  
Mengyi Du ◽  
Lu Tang ◽  
Jie Zhou ◽  
...  
Keyword(s):  
Bacterial Translocation ◽  
Disseminated Intravascular Coagulation ◽  
Intestinal Barrier ◽  
Plasminogen Activator Inhibitor ◽  
Coagulation Factors ◽  
Organ Damage ◽  
Multiple Organ ◽  
Plasminogen Activator Inhibitor 1 ◽  
Intravascular Coagulation ◽  
Coagulation Dysfunction

Abstract Background: Disseminated intravascular coagulation (DIC) is characterized by extensive endothelial injury and coagulation activation that is primarily caused by infection and can be aggravated by the gut due to increased permeability and bacterial translocation. Studies have shown that statins play an important role in reducing inflammation, protecting the endothelium and improving coagulation. In addition, statins regulate tight junction (TJ) proteins and gut microbes. Therefore, we aimed to investigate whether simvastatin improves DIC prognosis by regulating the intestinal microenvironment. Methods: Mice were administered 20 mg/kg simvastatin by gavage for 2 weeks and then intraperitoneally injected with 50 mg/kg endotoxin. Twelve hours later, cytokine release, coagulation dysfunction, multiple organ damage and survival were assessed. In addition, intestinal barrier and permeability and bacteria and bacteria translocation were evaluated. Results: We found that the severity of endotoxin-induced DIC was significantly improved in simvastatin-pretreated mice, who showed attenuated depletion of coagulation factors and platelets, decreased plasminogen activator inhibitor-1 (PAI-1) expression, reduced organ fibrin deposition and an improved survival rate. In addition, simvastatin reduced epithelial apoptosis, increased TJ gene expression, and upregulated antimicrobial peptides, lysozyme and mucins. Simvastatin-pretreated mice showed increased Lactobacillales counts, while the LPS group had increased numbers of Desulfovibrio and Mucispirillum, which produce harmful toxins and damage the intestinal epithelium and mucosa. Finally, with the decreased intestinal permeability in the simvastatin group, bacterial translocation in the organs and blood was significantly reduced, both in quantity and species. Conclusions: Simvastatin improves DIC prognosis, and the intestinal microenvironment participates in this process.

Measuring tissue factor (factor III) activity in plasma.

1989 ◽  
Vol 35 (9) ◽  
pp. 1897-1900 ◽  
Author(s):  
C Fukuda ◽  
K Iijima ◽  
K Nakamura
Keyword(s):  
Tissue Factor ◽  
Disseminated Intravascular Coagulation ◽  
Coagulation Factors ◽  
High Plasma ◽  
Mean Value ◽  
Chromogenic Substrate ◽  
Intravascular Coagulation ◽  
Endogenous Inhibitors ◽  
Tissue Thromboplastin ◽  
The Mean

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.

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