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1.
Int J Mol Sci ; 23(6)2022 Mar 19.
Article in English | MEDLINE | ID: covidwho-1760654

ABSTRACT

Coronavirus Disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and is frequently complicated by thrombosis. In some cases of severe COVID-19, fibrinolysis may be markedly enhanced within a few days, resulting in fatal bleeding. In the treatment of COVID-19, attention should be paid to both coagulation activation and fibrinolytic activation. Various thromboses are known to occur after vaccination with SARS-CoV-2 vaccines. Vaccine-induced immune thrombotic thrombocytopenia (VITT) can occur after adenovirus-vectored vaccination, and is characterized by the detection of anti-platelet factor 4 antibodies by enzyme-linked immunosorbent assay and thrombosis in unusual locations such as cerebral venous sinuses and visceral veins. Treatment comprises high-dose immunoglobulin, argatroban, and fondaparinux. Some VITT cases show marked decreases in fibrinogen and platelets and marked increases in D-dimer, suggesting the presence of enhanced-fibrinolytic-type disseminated intravascular coagulation with a high risk of bleeding. In the treatment of VITT, evaluation of both coagulation activation and fibrinolytic activation is important, adjusting treatments accordingly to improve outcomes.


Subject(s)
Blood Coagulation Disorders/etiology , COVID-19 Vaccines/adverse effects , COVID-19/complications , SARS-CoV-2 , Biomarkers , Blood Coagulation , Blood Coagulation Disorders/diagnosis , Blood Coagulation Disorders/prevention & control , Blood Coagulation Disorders/therapy , Blood Coagulation Tests , COVID-19/immunology , COVID-19/prevention & control , COVID-19 Vaccines/immunology , Combined Modality Therapy , Disease Management , Disease Susceptibility , Fibrinolysis , Humans , Prognosis , Treatment Outcome
2.
Int J Mol Sci ; 23(3)2022 Jan 24.
Article in English | MEDLINE | ID: covidwho-1686810

ABSTRACT

Aortic aneurysms are sometimes associated with enhanced-fibrinolytic-type disseminated intravascular coagulation (DIC). In enhanced-fibrinolytic-type DIC, both coagulation and fibrinolysis are markedly activated. Typical cases show decreased platelet counts and fibrinogen levels, increased concentrations of fibrin/fibrinogen degradation products (FDP) and D-dimer, and increased FDP/D-dimer ratios. Thrombin-antithrombin complex or prothrombin fragment 1 + 2, as markers of coagulation activation, and plasmin-α2 plasmin inhibitor complex, a marker of fibrinolytic activation, are all markedly increased. Prolongation of prothrombin time (PT) is not so obvious, and the activated partial thromboplastin time (APTT) is rather shortened in some cases. As a result, DIC can be neither diagnosed nor excluded based on PT and APTT alone. Many of the factors involved in coagulation and fibrinolysis activation are serine proteases. Treatment of enhanced-fibrinolytic-type DIC requires consideration of how to control the function of these serine proteases. The cornerstone of DIC treatment is treatment of the underlying pathology. However, in some cases surgery is either not possible or exacerbates the DIC associated with aortic aneurysm. In such cases, pharmacotherapy becomes even more important. Unfractionated heparin, other heparins, synthetic protease inhibitors, recombinant thrombomodulin, and direct oral anticoagulants (DOACs) are agents that inhibit serine proteases, and all are effective against DIC. Inhibition of activated coagulation factors by anticoagulants is key to the treatment of DIC. Among them, DOACs can be taken orally and is useful for outpatient treatment. Combination therapy of heparin and nafamostat allows fine-adjustment of anticoagulant and antifibrinolytic effects. While warfarin is an anticoagulant, this agent is ineffective in the treatment of DIC because it inhibits the production of coagulation factors as substrates without inhibiting activated coagulation factors. In addition, monotherapy using tranexamic acid in cases of enhanced-fibrinolytic-type DIC may induce fatal thrombosis. If tranexamic acid is needed for DIC, combination with anticoagulant therapy is of critical importance.


Subject(s)
Aortic Aneurysm/complications , Disseminated Intravascular Coagulation/therapy , Fibrinolysis/drug effects , Anticoagulants/pharmacology , Antifibrinolytic Agents/blood , Fibrin Fibrinogen Degradation Products , Fibrinolysin , Fibrinolysis/physiology , Heparin/pharmacology , Humans , Partial Thromboplastin Time , Prothrombin Time , alpha-2-Antiplasmin
3.
Non-conventional in English | MEDLINE, Grey literature | ID: grc-750559
5.
Int J Hematol ; 113(1): 45-57, 2021 Jan.
Article in English | MEDLINE | ID: covidwho-1064611

ABSTRACT

The pathology of coronavirus disease 2019 (COVID-19) is exacerbated by the progression of thrombosis, and disseminated intravascular coagulation (DIC), and cytokine storms. The most frequently reported coagulation/fibrinolytic abnormality in COVID-19 is the increase in D-dimer, and its relationship with prognosis has been discussed. However, limits exist to the utility of evaluation by D-dimer alone. In addition, since the coagulation/fibrinolytic condition sometimes fluctuates within a short period of time, regular examinations in recognition of the significance of the examination are desirable. The pathophysiology of disseminated intravascular coagulation (DIC) associated with COVID-19 is very different from that of septic DIC, and both thrombotic and hemorrhagic pathologies should be noted. COVID-19 thrombosis includes macro- and microthrombosis, with diagnosis of the latter depending on markers of coagulation and fibrinolysis. Treatment of COVID-19 is classified into antiviral treatment, cytokine storm treatment, and thrombosis treatment. Rather than providing uniform treatment, the treatment method most suitable for the severity and stage should be selected. Combination therapy with heparin and nafamostat is expected to develop in the future. Fibrinolytic therapy and adsorption therapy require further study.


Subject(s)
Blood Coagulation Disorders/etiology , COVID-19/blood , Pandemics , SARS-CoV-2 , Adult , Anticoagulants/therapeutic use , Benzamidines , Blood Coagulation Disorders/physiopathology , Blood Coagulation Tests , COVID-19/complications , COVID-19/drug therapy , COVID-19/mortality , COVID-19/therapy , Cytokine Release Syndrome/blood , Cytokine Release Syndrome/drug therapy , Cytokine Release Syndrome/etiology , Disseminated Intravascular Coagulation/etiology , Disseminated Intravascular Coagulation/physiopathology , Female , Fibrin Fibrinogen Degradation Products/analysis , Fibrinolysis , Guanidines/pharmacology , Guanidines/therapeutic use , Humans , Lymphopenia/etiology , Male , Middle Aged , Prognosis , Pulmonary Circulation , SARS-CoV-2/drug effects , Survivors , Thrombocytopenia/etiology , Thrombophilia/drug therapy , Thrombophilia/etiology , Thrombophilia/physiopathology
8.
Japanese Journal of Thrombosis and Hemostasis ; 31(6):604-618, 2020.
Article in English | J-STAGE | ID: covidwho-976157
9.
Int J Hematol ; 113(1): 45-57, 2021 Jan.
Article in English | MEDLINE | ID: covidwho-915246

ABSTRACT

The pathology of coronavirus disease 2019 (COVID-19) is exacerbated by the progression of thrombosis, and disseminated intravascular coagulation (DIC), and cytokine storms. The most frequently reported coagulation/fibrinolytic abnormality in COVID-19 is the increase in D-dimer, and its relationship with prognosis has been discussed. However, limits exist to the utility of evaluation by D-dimer alone. In addition, since the coagulation/fibrinolytic condition sometimes fluctuates within a short period of time, regular examinations in recognition of the significance of the examination are desirable. The pathophysiology of disseminated intravascular coagulation (DIC) associated with COVID-19 is very different from that of septic DIC, and both thrombotic and hemorrhagic pathologies should be noted. COVID-19 thrombosis includes macro- and microthrombosis, with diagnosis of the latter depending on markers of coagulation and fibrinolysis. Treatment of COVID-19 is classified into antiviral treatment, cytokine storm treatment, and thrombosis treatment. Rather than providing uniform treatment, the treatment method most suitable for the severity and stage should be selected. Combination therapy with heparin and nafamostat is expected to develop in the future. Fibrinolytic therapy and adsorption therapy require further study.


Subject(s)
Blood Coagulation Disorders/etiology , COVID-19/blood , Pandemics , SARS-CoV-2 , Adult , Anticoagulants/therapeutic use , Benzamidines , Blood Coagulation Disorders/physiopathology , Blood Coagulation Tests , COVID-19/complications , COVID-19/drug therapy , COVID-19/mortality , COVID-19/therapy , Cytokine Release Syndrome/blood , Cytokine Release Syndrome/drug therapy , Cytokine Release Syndrome/etiology , Disseminated Intravascular Coagulation/etiology , Disseminated Intravascular Coagulation/physiopathology , Female , Fibrin Fibrinogen Degradation Products/analysis , Fibrinolysis , Guanidines/pharmacology , Guanidines/therapeutic use , Humans , Lymphopenia/etiology , Male , Middle Aged , Prognosis , Pulmonary Circulation , SARS-CoV-2/drug effects , Survivors , Thrombocytopenia/etiology , Thrombophilia/drug therapy , Thrombophilia/etiology , Thrombophilia/physiopathology
10.
Int J Infect Dis ; 102: 529-531, 2021 Jan.
Article in English | MEDLINE | ID: covidwho-898988

ABSTRACT

Nafamostat, a serine proteinase inhibitor with various actions including antithrombin, antiplasmin, and antitrypsin effects, has been used in clinical practice to treat disseminated intravascular coagulation (DIC) and pancreatitis. This case report describes the clinical course of a patient with COVID-19 pneumonia whose severe hypoxemia, probably caused by DIC and pulmonary embolism, showed remarkable improvement with combination heparin and nafamostat therapy. In addition, beneficial mechanisms of nafamostat against COVID-19 and the necessity of attention to hyperkalemia as an adverse effect are discussed.


Subject(s)
Anticoagulants/administration & dosage , COVID-19/complications , Disseminated Intravascular Coagulation/drug therapy , Guanidines/administration & dosage , Aged , Benzamidines , Blood Coagulation/drug effects , COVID-19/blood , COVID-19/virology , Disseminated Intravascular Coagulation/blood , Disseminated Intravascular Coagulation/etiology , Disseminated Intravascular Coagulation/virology , Humans , Male , SARS-CoV-2/physiology
12.
J Intensive Care ; 8: 71, 2020.
Article in English | MEDLINE | ID: covidwho-781556

ABSTRACT

A high rate of thrombotic complications, such as pulmonary embolism, has been linked to mortality in COVID-19, and appropriate treatment of thrombosis is important for lifesaving. Although heparin is frequently used to treat thrombotic pathology in COVID-19, pulmonary embolism is still seen in severe cases. Although systemic fibrinolytic therapy is a focus of attention because a thrombotic pathology is the cause of death in severe COVID-19, it should be kept in mind that fibrinolytic therapy might be harmful at advanced stage of COVID-19 where the status of disseminated intravascular coagulation (DIC) has been transmitted from suppressed-fibrinolytic to enhanced-fibrinolytic in disease progression of COVID-19. In this respect, inhalation therapy with fibrinolytic substances might be a safe and promising treatment.

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