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  1. Article ; Online: Platelets and the Endothelium: Active Participants in Severe COVID-19 Infection.

    Parker, William A E / Storey, Robert F

    JACC. Basic to translational science

    2021  Volume 6, Issue 3, Page(s) 219–221

    Language English
    Publishing date 2021-03-22
    Publishing country United States
    Document type Editorial ; Comment
    ISSN 2452-302X
    ISSN (online) 2452-302X
    DOI 10.1016/j.jacbts.2021.01.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Uncoupling of platelet granule release and integrin activation suggests GPIIb/IIIa as a therapeutic target in COVID-19.

    Weiss, Lukas J / Drayss, Maria / Manukjan, Georgi / Zeitlhöfler, Maximilian / Kleiss, Judith / Weigel, Mathis / Herrmann, Johannes / Mott, Kristina / Beck, Sarah / Burkard, Philipp / Lâm, Thiên-Trí / Althaus, Karina / Bakchoul, Tamam / Frantz, Stefan / Meybohm, Patrick / Nieswandt, Bernhard / Weismann, Dirk / Schulze, Harald

    Blood advances

    2022  Volume 7, Issue 11, Page(s) 2324–2338

    Abstract: ... in COVID-19 and sepsis samples under venous shear rates, which was dependent on the presence of tissue ... Thromboembolic events are frequent and life-threating complications of COVID-19 but are also ... From hospital admission onward, platelets in COVID-19 failed to activate the integrin glycoprotein IIb/IIa ...

    Abstract Thromboembolic events are frequent and life-threating complications of COVID-19 but are also observed in patients with sepsis. Disseminated thrombosis can occur despite anticoagulation, suggesting that platelets play a direct but incompletely understood role. Several studies demonstrated altered platelet function in COVID-19 with some controversial findings, while underlying disease-specific mechanisms remain ill defined. We performed a comprehensive cohort study with 111 patients, comprising 37 with COVID-19, 46 with sepsis, and 28 with infection, compared with control participants. Platelet phenotype and function were assessed under static and flow conditions, revealing unexpected disease-specific differences. From hospital admission onward, platelets in COVID-19 failed to activate the integrin glycoprotein IIb/IIa (GPIIb/IIIa) in response to multiple agonists. Dense granule release was markedly impaired due to virtually missing granules, also demonstrated by whole-mount electron microscopy. By contrast, α-granule marker CD62P exposure was only mildly affected, revealing a subpopulation of PAC-1-/CD62P+ platelets, independently confirmed by automated clustering. This uncoupling of α-granule release was not observed in patients with sepsis, despite a similar disease severity. We found overall unaltered thrombus formation in COVID-19 and sepsis samples under venous shear rates, which was dependent on the presence of tissue factor. Unexpectedly, under arterial shear rates, thrombus formation was virtually abrogated in sepsis, whereas we detected overall normal-sized and stable thrombi in blood from patients with COVID-19. These thrombi were susceptible to subthreshold levels of GPIIb/IIIa blockers, eptifibatide, or tirofiban that had only a minor effect in control participants' blood. We provide evidence that low-dose GPIIb/IIIa blockade could be a therapeutic approach in COVID-19.
    MeSH term(s) Humans ; Platelet Aggregation Inhibitors/therapeutic use ; Platelet Glycoprotein GPIIb-IIIa Complex ; Cohort Studies ; COVID-19 ; Thrombosis/drug therapy ; Thrombosis/etiology ; Sepsis
    Chemical Substances Platelet Aggregation Inhibitors ; Platelet Glycoprotein GPIIb-IIIa Complex
    Language English
    Publishing date 2022-08-29
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2915908-8
    ISSN 2473-9537 ; 2473-9529
    ISSN (online) 2473-9537
    ISSN 2473-9529
    DOI 10.1182/bloodadvances.2022008666
    Database MEDical Literature Analysis and Retrieval System OnLINE

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