Journal of thrombosis and haemostasis : JTH
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J. Thromb. Haemost. · Aug 2020
Comparative StudyIncidence of venous thromboembolism in hospitalized patients with COVID-19.
Coronavirus disease 2019 (COVID-19) can lead to systemic coagulation activation and thrombotic complications. ⋯ The observed risk for VTE in COVID-19 is high, particularly in ICU patients, which should lead to a high level of clinical suspicion and low threshold for diagnostic imaging for DVT or PE. Future research should focus on optimal diagnostic and prophylactic strategies to prevent VTE and potentially improve survival.
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The COVID-19 pandemic has become an urgent issue in every country. Based on recent reports, the most severely ill patients present with coagulopathy, and disseminated intravascular coagulation (DIC)-like massive intravascular clot formation is frequently seen in this cohort. Therefore, coagulation tests may be considered useful to discriminate severe cases of COVID-19. ⋯ The mechanisms of the coagulopathy are not fully elucidated, however. It is speculated that the dysregulated immune responses orchestrated by inflammatory cytokines, lymphocyte cell death, hypoxia, and endothelial damage are involved. Bleeding tendency is uncommon, but the incidence of thrombosis in COVID-19 and the adequacy of current recommendations regarding standard venous thromboembolic dosing are uncertain.
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J. Thromb. Haemost. · Dec 2020
ReviewDiverse activities of von Willebrand factor in traumatic brain injury and associated coagulopathy.
Traumatic brain injury (TBI) is a leading cause of death and disability. Patients with isolated TBI lose a limited amount of blood to primary injury, but they often develop secondary coagulopathy, resulting in delayed or recurrent intracranial and intracerebral hematoma. TBI-induced coagulopathy is closely associated with poor outcomes for these patients, including death. ⋯ A key question is how a localized injury to the brain is rapidly disseminated to affect systemic hemostasis that is not directly affected the way it is in trauma to the body and limbs, especially with hemorrhagic shock. Increasing evidence suggests that the adhesive ligand von Willebrand factor (VWF), which is synthesized in and released from endothelial cells, plays a paradoxical role in both facilitating local hemostasis at the site of injury and also propagating TBI-induced endotheliopathy and coagulopathy systemically. This review discusses recent progress in understanding these diverse activities of VWF and the knowledge gaps in defining their roles in TBI and associated coagulopathy.
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Clinical Trial Controlled Clinical Trial
Thromboprophylaxis improves the live birth rate in women with consecutive recurrent miscarriages and hereditary thrombophilia.
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J. Thromb. Haemost. · Sep 2020
ReviewCOVID-19: A collision of complement, coagulation and inflammatory pathways.
COVID-19 is frequently accompanied by a hypercoagulable inflammatory state with microangiopathic pulmonary changes that can precede the diffuse alveolar damage characteristic of typical acute respiratory distress syndrome (ARDS) seen in other severe pathogenic infections. Parallels with systemic inflammatory disorders such as atypical hemolytic uremic syndrome (aHUS) have implicated the complement pathway in the pathogenesis of COVID-19, and particularly the anaphylatoxins C3a and C5a released from cleavage of C3 and C5, respectively. C5a is a potent cell signalling protein that activates a cytokine storm-a hyper-inflammatory phenomenon-within hours of infection and the innate immune response. ⋯ Pathologic studies report strong evidence of complement activation. C5 blockade reduces inflammatory cytokines and their manifestations in animal studies, and has shown benefits in patients with aHUS, prompting investigation of this approach in the treatment of COVID-19. This review describes the role of the complement pathway and particularly C5a and its aberrations in highly pathogenic virus infections, and therefore its potential as a therapeutic target in COVID-19.