Mary Wilson
Well-known member
29 June 2021
https://doi.org/10.7326/M21-2680
Allyson M. Pishko, MD, Adam Cuker, MD, MS
Vaccine-induced thrombosis and thrombocytopenia (VITT), also referred to as thrombosis with thrombocytopenia syndrome, is a rare and potentially life-threatening disorder described in previously healthy persons after receipt of 1 of 2 adenovirus-based SARS-CoV-2 vaccines (AstraZeneca [ChAdOx1] or Johnson & Johnson [Ad26.COV2.S]) (1). The syndrome is characterized by moderate to severe thrombocytopenia and thrombosis, generally occurring 5 to 30 days after vaccine administration. Thrombosis in atypical locations, particularly the cerebral venous sinuses and splanchnic veins, is a hallmark of the disorder (1).
Although the mechanism of VITT has only begun to be elucidated, it seems similar to but also distinct from heparin-induced thrombocytopenia (HIT) in certain respects. In both VITT and HIT, IgG antibodies bind to platelet factor 4 (PF4) on the surface of platelets, resulting in widespread platelet activation. Indeed, antibodies to complexes of PF4 and polyanion (“HIT antibodies”) have been detected in most of the confirmed cases of VITT by enzyme-linked immunosorbent assays, typically at high titers (>1.0 optical density [OD] units) (1). However, unlike HIT, VITT occurs in the absence of antecedent heparin exposure, and VITT antibodies do not depend on the presence of heparin to bind PF4 and activate platelets.
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https://www.acpjournals.org/doi/10.7326/M21-2680
https://doi.org/10.7326/M21-2680
Allyson M. Pishko, MD, Adam Cuker, MD, MS
Vaccine-induced thrombosis and thrombocytopenia (VITT), also referred to as thrombosis with thrombocytopenia syndrome, is a rare and potentially life-threatening disorder described in previously healthy persons after receipt of 1 of 2 adenovirus-based SARS-CoV-2 vaccines (AstraZeneca [ChAdOx1] or Johnson & Johnson [Ad26.COV2.S]) (1). The syndrome is characterized by moderate to severe thrombocytopenia and thrombosis, generally occurring 5 to 30 days after vaccine administration. Thrombosis in atypical locations, particularly the cerebral venous sinuses and splanchnic veins, is a hallmark of the disorder (1).
Although the mechanism of VITT has only begun to be elucidated, it seems similar to but also distinct from heparin-induced thrombocytopenia (HIT) in certain respects. In both VITT and HIT, IgG antibodies bind to platelet factor 4 (PF4) on the surface of platelets, resulting in widespread platelet activation. Indeed, antibodies to complexes of PF4 and polyanion (“HIT antibodies”) have been detected in most of the confirmed cases of VITT by enzyme-linked immunosorbent assays, typically at high titers (>1.0 optical density [OD] units) (1). However, unlike HIT, VITT occurs in the absence of antecedent heparin exposure, and VITT antibodies do not depend on the presence of heparin to bind PF4 and activate platelets.
...
https://www.acpjournals.org/doi/10.7326/M21-2680