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      Thrombosis and Thrombocytopenia after ChAdOx1 nCoV-19 Vaccination

      , M.D., Ph.D., , M.D., , Ph.D., , M.D., Ph.D., , M.D., Ph.D., , Ph.D., , M.D., Ph.D., , M.D., Ph.D., , M.D., , M.D., Ph.D., , M.D., Ph.D.
      The New England Journal of Medicine
      Massachusetts Medical Society
      Keyword part (code): 2Keyword part (keyword): Hematology/OncologyKeyword part (code): 2_3Keyword part (keyword): Coagulation , 2, Hematology/Oncology, Keyword part (code): 2_3Keyword part (keyword): Coagulation, 2_3, Coagulation, Keyword part (code): 14Keyword part (keyword): CardiologyKeyword part (code): 14_5Keyword part (keyword): Anticoagulation/Thromboembolism , 14, Cardiology, Keyword part (code): 14_5Keyword part (keyword): Anticoagulation/Thromboembolism, 14_5, Anticoagulation/Thromboembolism, Keyword part (code): 18Keyword part (keyword): Infectious DiseaseKeyword part (code): 18_2Keyword part (keyword): VaccinesKeyword part (code): 18_6Keyword part (keyword): Viral Infections , 18, Infectious Disease, Keyword part (code): 18_2Keyword part (keyword): VaccinesKeyword part (code): 18_6Keyword part (keyword): Viral Infections , 18_2, Vaccines, 18_6, Viral Infections

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          We report findings in five patients who presented with venous thrombosis and thrombocytopenia 7 to 10 days after receiving the first dose of the ChAdOx1 nCoV-19 adenoviral vector vaccine against coronavirus disease 2019 (Covid-19). The patients were health care workers who were 32 to 54 years of age. All the patients had high levels of antibodies to platelet factor 4–polyanion complexes; however, they had had no previous exposure to heparin. Because the five cases occurred in a population of more than 130,000 vaccinated persons, we propose that they represent a rare vaccine-related variant of spontaneous heparin-induced thrombocytopenia that we refer to as vaccine-induced immune thrombotic thrombocytopenia.

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          Autoimmune heparin-induced thrombocytopenia.

          Autoimmune heparin-induced thrombocytopenia (aHIT) indicates the presence in patients of anti-platelet factor 4 (PF4)-polyanion antibodies that are able to activate platelets strongly even in the absence of heparin (heparin-independent platelet activation). Nevertheless, as seen with serum obtained from patients with otherwise typical heparin-induced thrombocytopenia (HIT), serum-induced platelet activation is inhibited at high heparin concentrations (10-100 IU mL-1heparin). Furthermore, upon serial dilution, aHIT serum will usually show heparin-dependent platelet activation. Clinical syndromes associated with aHIT include: delayed-onset HIT, persisting HIT, spontaneous HIT syndrome, fondaparinux-associated HIT, heparin 'flush'-induced HIT, and severe HIT (platelet count of < 20 × 109 L-1) with associated disseminated intravascular coagulation (DIC). Recent studies have implicated anti-PF4 antibodies that are able to bridge two PF4 tetramers even in the absence of heparin, probably facilitated by non-heparin platelet-associated polyanions (chondroitin sulfate and polyphosphates); nascent PF4-aHIT-IgG complexes recruit additional heparin-dependent HIT antibodies, leading to the formation of large multimolecular immune complexes and marked platelet activation. aHIT can persist for several weeks, and serial fibrin, D-dimer, and fibrinogen levels, rather than the platelet count, may be helpful for monitoring treatment response. Although standard anticoagulant therapy for HIT ought to be effective, published experience indicates frequent failure of activated partial thromboplastin time (APTT)-adjusted anticoagulants (argatroban, bivalirudin), probably because of underdosing in the setting of HIT-associated DIC, known as 'APTT confounding'. Thus, non-APTT-adjusted therapies with drugs such as danaparoid and fondaparinux, or even direct oral anticoagulants, such as rivaroxaban or apixaban, are suggested therapies, especially for long-term management of persisting HIT. In addition, emerging data indicate that high-dose intravenous immunoglobulin can interrupt HIT antibody-induced platelet activation, leading to rapid platelet count recovery.
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            Is Open Access

            Systemic complement activation is associated with respiratory failure in COVID-19 hospitalized patients

            Significance The new SARS-CoV-2 pandemic leads to COVID-19 with respiratory failure, substantial morbidity, and significant mortality. Overactivation of the innate immune response is postulated to trigger this detrimental process. The complement system is a key player in innate immunity. Despite a few reports of local complement activation, there is a lack of evidence that the degree of systemic complement activation occurs early in COVID-19 patients, and whether this is associated with respiratory failure. This study shows that a number of complement activation products are systemically, consistently, and long-lastingly increased from admission and during the hospital stay. Notably, the terminal sC5b-9 complement complex was associated with respiratory failure. Thus, complement inhibition is an attractive therapeutic approach for treatment of COVD-19.
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                Author and article information

                N Engl J Med
                N Engl J Med
                The New England Journal of Medicine
                Massachusetts Medical Society
                09 April 2021
                From the Departments of Hematology (N.H.S., G.E.T., P.A.H.), Immunology (L.A.M., F.L.-J.), Neurosurgery (M.W.), Neurology (A.-H.A.), and Radiology and Nuclear Medicine (T.H.S.), and the Research Institute of Internal Medicine (N.H.S., A.E.M., P.A.H.), Oslo University Hospital, and the Faculty of Medicine (A.E.M., G.E.T., P.A.H.), the KG Jebsen Center for B Cell Malignancy (L.A.M., G.E.T.), Institute of Clinical Medicine, and the ImmunoLingo Convergence Center (F.L.-J.), University of Oslo, the Department of Hematology, Akershus University Hospital, Lørenskog (N.H.S.), and the Norwegian National Unit for Platelet Immunology, Division of Diagnostics, University Hospital of North Norway, Tromsø (I.H.S., M.T.A.) — all in Norway.
                Author notes
                Address reprint requests to Dr. Holme at the Department of Hematology, Oslo University Hospital, Rikshospitalet, Postbox 4950, N-0424 Oslo, Norway, or at pholme@ 123456ous-hf.no .
                Copyright © 2021 Massachusetts Medical Society. All rights reserved.

                This article is made available via the PMC Open Access Subset for unrestricted re-use, except commercial resale, and analyses in any form or by any means with acknowledgment of the original source. These permissions are granted for the duration of the Covid-19 pandemic or until revoked in writing. Upon expiration of these permissions, PMC is granted a license to make this article available via PMC and Europe PMC, subject to existing copyright protections.

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