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10.1111/jth.15262

http://scihub22266oqcxt.onion/10.1111/jth.15262
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33550713!8013750!33550713
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suck abstract from ncbi


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pmid33550713      J+Thromb+Haemost 2021 ; 19 (5): 1294-1298
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  • COVID-19 patients often show high-titer non-platelet-activating anti-PF4/heparin IgG antibodies #MMPMID33550713
  • Brodard J; Kremer Hovinga JA; Fontana P; Studt JD; Gruel Y; Greinacher A
  • J Thromb Haemost 2021[May]; 19 (5): 1294-1298 PMID33550713show ga
  • BACKGROUND: Heparin-induced thrombocytopenia (HIT) is a severe adverse reaction to heparin caused by heparin-dependent, platelet-activating anti-platelet factor 4 (PF4)/heparin antibodies. Heparin is a cornerstone of treatment in critically ill COVID-19 patients. HIT antibodies can be detected by antigen tests and functional tests. Often strong reactivity in the antigen test is used as a surrogate marker for the presence of clinically relevant, platelet-activating antibodies. We observed an unexpectedly high percentage of COVID-19 patients, clinically suspected to have HIT, with high titer anti-PF4/heparin antibodies, but a negative functional test. OBJECTIVE: We investigated whether in COVID-19 patients a serum-derived factor inhibits the heparin-induced platelet activation test (HIPA). METHODS AND RESULTS: Twelve COVID-19 patients with suspected HIT were tested. Three samples tested negative in all assays; nine samples tested positive by antigen tests, among which only three tested also positive by HIPA. When we spiked COVID-19 serum or control serum with the human HIT antibody like monoclonal antibody 5B9, reactivity of 5B9 remained the same. Also, the purified IgG fractions of COVID-19 sera testing strongly positive in the PF4/heparin antigen test but negative in the functional test did not show increased reactivity in the functional test in comparison to the original serum. Both results make a functionally inhibitory factor in the serum/plasma of COVID-19 patients highly unlikely. CONCLUSION: COVID-19 patients often present with strong reactivity in PF4/heparin antigen tests without the presence of platelet-activating antibodies. Diagnosis of HIT requires confirmation of heparin-dependent, platelets activating antibodies to avoid overdiagnosis and overtreatment with non-heparin anticoagulants.
  • |*COVID-19[MESH]
  • |*Heparin/adverse effects[MESH]
  • |Anticoagulants[MESH]
  • |Blood Platelets[MESH]
  • |Humans[MESH]
  • |Immunoglobulin G[MESH]
  • |Platelet Factor 4[MESH]


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