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1.
J Thromb Haemost ; 18(9): 2430-2432, 2020 09.
Article in English | MEDLINE | ID: covidwho-659577
2.
J Thromb Haemost ; 18(9): 2118-2122, 2020 09.
Article in English | MEDLINE | ID: covidwho-599236

ABSTRACT

The COVID-19 pandemic has provided many challenges in the field of thrombosis and hemostasis. Among these is a novel form of coagulopathy that includes exceptionally high levels of D-dimer. D-dimer is a marker of poor prognosis, but does this also imply a causal relationship? These spectacularly raised D-dimer levels may actually signify the failing attempt of the fibrinolytic system to remove fibrin and necrotic tissue from the lung parenchyma, being consumed or overwhelmed in the process. Indeed, recent studies suggest that increasing fibrinolytic activity might offer hope for patients with critical disease and severe respiratory failure. However, the fibrinolytic system can also be harnessed by coronavirus to promote infectivity and where antifibrinolytic measures would also seem appropriate. Hence, there is a clinical paradox where plasmin formation can be either deleterious or beneficial in COVID-19, but not at the same time. Hence, it all comes down to timing.


Subject(s)
COVID-19 Drug Treatment , COVID-19/blood , COVID-19/complications , Fibrinolysis/drug effects , Acute Lung Injury , Animals , Antifibrinolytic Agents/pharmacology , Fibrin/metabolism , Fibrin Fibrinogen Degradation Products/metabolism , Fibrinolysin/metabolism , Humans , Immune System , Lung/metabolism , Necrosis , Prognosis , Thrombolytic Therapy , Tissue Plasminogen Activator/pharmacology
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