Perspective on fibrinolytic therapy in COVID-19: the potential of inhalation therapy against suppressed-fibrinolytic-typ
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(2020) 8:71
LETTER TO THE EDITOR
Open Access
Perspective on fibrinolytic therapy in COVID-19: the potential of inhalation therapy against suppressed-fibrinolytic-type DIC Hidesaku Asakura1* and Haruhiko Ogawa2
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 enhancedfibrinolytic in disease progression of COVID-19. In this respect, inhalation therapy with fibrinolytic substances might be a safe and promising treatment. Keywords: COVID-19, Thrombosis, Fibrinolytic therapy
Fibrinolytic therapy for pulmonary intravascular coagulation in coronavirus disease 2019 (COVID-19) Some articles suggest several treatment options using fibrinolytic drugs for acute respiratory distress syndrome (ARDS) in severe cases of COVID-19 [1–4]. ARDS and organ dysfunction associated with a cytokine storm have been identified as causes of death in COVID-19 [5]. In addition, a high rate of thrombotic complications, such as pulmonary embolism, has been linked to mortality. Interestingly, despite the presence of systemic hypercoagulation associated with the strong inflammation in severe COVID-19, the site of thrombosis was the lungs in the overwhelming majority of cases. These were not only cases of pulmonary embolism diagnosed by methods such as contrast computed tomography, but included * Correspondence: [email protected] 1 Department of Hematology, Kanazawa University Hospital, Takaramachi 13-1, Kanazawa, Ishikawa 920-8640, Japan Full list of author information is available at the end of the article
microscopic fibrin thrombosis that was frequently seen at the level of the pulmonary microcirculation in autopsy investigations [6–8]. The pulmonary thrombosis in severe COVID-19 can be described as macroscopic and microscopic thrombosis. Although activation of coagulation is linked to a systemic cytokine storm, since the principal site of thrombus formation is the lungs, it might also be referred to as pulmonary intravascular coagulation [9]. COVID-19 patients with a high D-dimer level are known to have poor clinical outcomes, and this is thought to reflect a direct link between the thrombotic pathology and prognosis [10]. As Whyte et al. noted, exposure of tissue factors (TF) on damaged alveolar endothelial cells and on the surface of leukocytes promotes fibrin deposition. They also mentioned that significantly elevated expression of plasminogen activator inhibitor 1 (PAI-1) by lung epithelial and endothelial cells
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