A study reports that vaccination with the ChAdOx1 nCov-19 (AstraZeneca) vaccine can lead to a rare condition called immune thrombotic thrombocytopenia (ITT), characterized by thrombosis and thrombocytopenia. The condition is caused by platelet-activating antibodies against platelet factor 4 (PF4), which clinically resembles autoimmune heparin-induced thrombocytopenia (HIT). The study analyzed 11 patients in Germany and Austria who developed thrombotic events 5 to 16 days after vaccination. All patients had thrombocytopenia, with 9 having cerebral venous thrombosis, 3 having splanchnic-vein thrombosis, 3 having pulmonary embolism, and 4 having other thromboses. Five patients had disseminated intravascular coagulation. None of the patients had received heparin before symptom onset. All 28 patients who tested positive for PF4-heparin antibodies also tested positive on a platelet-activation assay in the presence of PF4, independent of heparin. Platelet activation was inhibited by high levels of heparin, Fc receptor-blocking monoclonal antibody, and immune globulin. Additional studies confirmed PF4-dependent platelet activation. The study concludes that vaccination with ChAdOx1 nCov-19 can result in the rare development of ITT mediated by platelet-activating antibodies against PF4, which clinically mimics HIT. The study was funded by the German Research Foundation.A study reports that vaccination with the ChAdOx1 nCov-19 (AstraZeneca) vaccine can lead to a rare condition called immune thrombotic thrombocytopenia (ITT), characterized by thrombosis and thrombocytopenia. The condition is caused by platelet-activating antibodies against platelet factor 4 (PF4), which clinically resembles autoimmune heparin-induced thrombocytopenia (HIT). The study analyzed 11 patients in Germany and Austria who developed thrombotic events 5 to 16 days after vaccination. All patients had thrombocytopenia, with 9 having cerebral venous thrombosis, 3 having splanchnic-vein thrombosis, 3 having pulmonary embolism, and 4 having other thromboses. Five patients had disseminated intravascular coagulation. None of the patients had received heparin before symptom onset. All 28 patients who tested positive for PF4-heparin antibodies also tested positive on a platelet-activation assay in the presence of PF4, independent of heparin. Platelet activation was inhibited by high levels of heparin, Fc receptor-blocking monoclonal antibody, and immune globulin. Additional studies confirmed PF4-dependent platelet activation. The study concludes that vaccination with ChAdOx1 nCov-19 can result in the rare development of ITT mediated by platelet-activating antibodies against PF4, which clinically mimics HIT. The study was funded by the German Research Foundation.