scholarly journals Detection of disseminated intravascular coagulation with the help of the conception of constant intravascular microcoagulation

2010 ◽  
Vol 138 (suppl. 1) ◽  
pp. 53-58
Author(s):  
Igor Bokarev ◽  
Ludmila Popova
Keyword(s):  
Blood Coagulation ◽  
19Th Century ◽  
High Mortality ◽  
Disseminated Intravascular Coagulation ◽  
Intravascular Coagulation ◽  
Number Of Patients ◽  
Arteries And Veins ◽  
Exact Diagnosis

The possibility of intravascular blood coagulation existence in the microvascular vessels and capillaries without the presence of a large thrombus in the arteries and veins has been known from the middle of 19th century. It is impossible to know exactly about the prevalence of this pathology, because there is a jumble in terminology that does not help statistics to be exact. One of the reasons of so high mortality from disseminated intravascular coagulation (DIC) is due to the impossibility to always make exact diagnosis, and as ?. Levi thinks it is provoked in the absence of generally accepted idea of DIC syndrome. We investigated these markers and the intensity of intravascular blood coagulation in a number of patients. Our understanding of the problems of DIC was formulated on the grounds of a thirty-year study of the problem involving over 1,500 patients. Thereby, the conception of constant intravascular microcoagulation (CIMC) was developed with the following aims: to report the existing material and bring to researchers and doctors in practice information about the presence of the phenomenon of CIMC and to resolve debatable questions of definitions and practical usage of up-to-date information about DIC with the help of CIMC conception.

scholarly journals Diagnosis and treatment of disseminated intravascular coagulation syndrome

2012 ◽  
Vol 93 (2) ◽  
pp. 364-366
Author(s):  
S V Kemerov
Keyword(s):  
Blood Coagulation ◽  
Disseminated Intravascular Coagulation ◽  
Treatment Strategy ◽  
Diagnostic Algorithm ◽  
Diagnosis And Treatment ◽  
Intravascular Coagulation

Disseminated intravascular blood coagulation syndrome is a rather complex pathology, accompanied by multi-directional shifts in the overall haemostasis. This article presents the diagnostic algorithm and treatment strategy, depending on the stage of disseminated intravascular blood coagulation syndrome.

scholarly journals Fatal case of acute fatty liver of pregnancy

2020 ◽  
Vol 10 (1) ◽  
pp. 410
Author(s):  
Sarada Mamilla ◽  
Sandhya Rani ◽  
Gayathri . ◽  
Bhavana . ◽  
Ramya Bharghavi ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Fatty Liver ◽  
High Mortality ◽  
Disseminated Intravascular Coagulation ◽  
Fatal Case ◽  
Mortality And Morbidity ◽  
Intravascular Coagulation ◽  
Acute Fatty Liver ◽  
In Pregnancy

Acute fatty liver in pregnancy is a catstrophic condition with high mortality and morbidity. Delay in managing complications would result in fatality. We present a case of 22-year-old primi, who presented to us in labor with jaundice and later developed, disseminated intravascular coagulation, Vulval haematoma, reexploration, sepsis, ARDS and cardiac arrest and death.

Recombinant Thrombomodulin and Activated Protein C in the Treatment of Disseminated Intravascular Coagulation

1999 ◽  
Vol 82 (08) ◽  
pp. 718-721 ◽  
Author(s):  
Ikuro Maruyama
Keyword(s):  
Endothelial Cells ◽  
Tissue Factor ◽  
Blood Coagulation ◽  
Disseminated Intravascular Coagulation ◽  
Protein C ◽  
Activated Protein C ◽  
Coagulation Cascade ◽  
Regulation System ◽  
Luminal Surface ◽  
Intravascular Coagulation

IntroductionThe blood coagulation cascade is regulated by the luminal surface of the endothelial cell lining.1 Endothelial cells synthesize tissue factor pathway inhibitor (TFPI), which, in part, binds to the cell surface glycosaminoglycans and inhibits factors Xa, VIIa, and tissue factor.2 Endothelial cells also produce and exhibit thrombomodulin (TM) on their luminal surface.3 TM is a kind of thrombin receptor that forms a 1:1 complex with thrombin. In this complex, thrombin activates protein C (PC) more than 1,000-fold more than thrombin alone. TM then loses its procoagulant activities, which include fibrinogen clotting, activation of factors V and VIII, and platelet activation. Thus, TM converts thrombin from a procoagulant protease to an anticoagulant. Pathologic states, such as an endothelial injury or perturbation or continuous rapid coagulation cascade activation, overcomes the endothelial regulating activity, resulting in the development of intravascular coagulation and the induction of disseminated intravascular coagulation (DIC). Theoretically, then, supplementing soluble TM or activated PC (APC) to reconstitute the endothelial coagulation regulation system in the circulation and regulate pathologically-activated blood coagulation could be beneficial. In this chapter, application of soluble TM and APC in the treatment of DIC is reviewed.

scholarly journals Thrombotic Thrombocytopenic Purpura— Coagulation Parameters in Twelve Patients

Blood ◽  
1973 ◽  
Vol 42 (4) ◽  
pp. 499-507 ◽  
Author(s):  
Eric A. Jaffe ◽  
Ralph L. Nachman ◽  
Clarence Merskey
Keyword(s):  
Blood Coagulation ◽  
Thrombotic Thrombocytopenic Purpura ◽  
Hemolytic Anemia ◽  
Disseminated Intravascular Coagulation ◽  
Temporal Relationship ◽  
Primary Factor ◽  
Thrombocytopenic Purpura ◽  
Intravascular Coagulation ◽  
Coagulation Abnormalities ◽  
Heparin Administration

Abstract Twelve patients with thrombotic thrombocytopenic purpura have been studied with emphasis on the changes in blood coagulation and the occurrence of disseminated intravascular coagulation (DIC). No coagulation abnormalities were found in six patients. Minimal abnormalities were present in three patients and major abnormalities compatible with DIC were present in three patients. There was little temporal relationship between the coagulation abnormalities and the clinical pathological course except for the extent of hemolysis. In addition, heparin administration in four patients had no effect on the course of the disease. Intravascular coagulation does not appear to be a primary factor in the pathogenesis of thrombotic thrombocytopenic purpura and the changes suggestive of DIC, when present, may well result from, rather than cause, the hemolytic anemia.

scholarly journals The effects of FUT-175 (nafamostat mesilate) on blood coagulation and experimental disseminated intravascular coagulation(DIC).

1987 ◽  
Vol 90 (6) ◽  
pp. 313-320 ◽  
Author(s):  
Yoshiko KOSHIYAMA ◽  
Akemi KOBORI ◽  
Madoka OGIHARA ◽  
Yasuki YOKOMOTO ◽  
Kyoko OHTANI ◽  
...  
Keyword(s):  
Blood Coagulation ◽  
Disseminated Intravascular Coagulation ◽  
Nafamostat Mesilate ◽  
Intravascular Coagulation

Disseminated intravascular coagulation and its immune mechanisms

Blood ◽  
2021 ◽  
Author(s):  
Narcis Ioan Popescu ◽  
Cristina Lupu ◽  
Florea Lupu
Keyword(s):  
Blood Coagulation ◽  
Disseminated Intravascular Coagulation ◽  
Clinical Manifestations ◽  
Regulatory Control ◽  
Intravascular Coagulation ◽  
Contact Pathway ◽  
Molecular Patterns ◽  
Endothelial Homeostasis ◽  
Damage Associated Molecular Patterns ◽  
New Strategies

Disseminated intravascular coagulation (DIC) is a syndrome triggered by infectious and non-infectious pathologies characterized by excessive generation of thrombin within the vasculature and widespread proteolytic conversion of fibrinogen. Despite diverse clinical manifestations ranging from thrombo-occlusive damage to bleeding diathesis, DIC etiology commonly involves excessive activation of blood coagulation and overlapping dysregulation of anticoagulants and fibrinolysis. Initiation of blood coagulation follows intravascular expression of tissue factor or activation of contact pathway in response to pathogen-associated or host derived damage-associated molecular patterns. The process is further amplified through inflammatory and immuno-thrombotic mechanisms. Consumption of anticoagulants and disruption of endothelial homeostasis lower the regulatory control and disseminate microvascular thrombosis. Clinical DIC development in patients associates with worsening morbidities and increased mortality regardless of the underlying pathology, therefore timely recognition of DIC is critical to reduce the pathologic burden. Due to diversity of triggers and pathogenic mechanisms leading to DIC, diagnosis is based on algorithms that quantify hemostatic imbalance, thrombocytopenia and fibrin/ogen conversion. Since current diagnosis primarily assesses overt consumptive coagulopathies, there is a critical need for better recognition of non-overt DIC and/or pre-DIC states. Therapeutic strategies for DIC patients involve resolution of the eliciting triggers and supportive care for the hemostatic imbalance. Despite medical care, mortality in DIC patients remains high and new strategies, tailored to the underlying pathologic mechanisms, are needed.

scholarly journals COVID-19-Related Coagulopathy—Is Transferrin a Missing Link?

Diagnostics ◽  
2020 ◽  
Vol 10 (8) ◽  
pp. 539 ◽  
Author(s):  
Katie-May McLaughlin ◽  
Marco Bechtel ◽  
Denisa Bojkova ◽  
Christian Münch ◽  
Sandra Ciesek ◽  
...  
Keyword(s):  
Gene Ontology ◽  
Blood Coagulation ◽  
Causative Agent ◽  
Disseminated Intravascular Coagulation ◽  
Tissue Expression ◽  
Gene Products ◽  
Binding Partner ◽  
Intravascular Coagulation ◽  
Expression Of Genes ◽  
Infected Cells

SARS-CoV-2 is the causative agent of COVID-19. Severe COVID-19 disease has been associated with disseminated intravascular coagulation and thrombosis, but the mechanisms underlying COVID-19-related coagulopathy remain unknown. The risk of severe COVID-19 disease is higher in males than in females and increases with age. To identify gene products that may contribute to COVID-19-related coagulopathy, we analyzed the expression of genes associated with the Gene Ontology (GO) term “blood coagulation” in the Genotype-Tissue Expression (GTEx) database and identified four procoagulants, whose expression is higher in males and increases with age (ADAMTS13, F11, HGFAC, KLKB1), and two anticoagulants, whose expression is higher in females and decreases with age (C1QTNF1, SERPINA5). However, the expression of none of these genes was regulated in a proteomics dataset of SARS-CoV-2-infected cells and none of the proteins have been identified as a binding partner of SARS-CoV-2 proteins. Hence, they may rather generally predispose individuals to thrombosis without directly contributing to COVID-19-related coagulopathy. In contrast, the expression of the procoagulant transferrin (not associated to the GO term “blood coagulation”) was higher in males, increased with age, and was upregulated upon SARS-CoV-2 infection. Hence, transferrin warrants further examination in ongoing clinic-pathological investigations.

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