COVID-19 vaccine-induced immune thrombotic thrombocytopenia

Abstract

The coronavirus disease (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus (SARS-CoV-2) stimulated the development of highly effective vaccines that were produced with unprecedented speed with the use of new technologies. All the newly developed vaccines are highly effective with minimal adverse effects. Clinical introduction of the AstraZeneca Covid-19 vaccine has raised public alarm regarding the rare, but serious thrombotic events, known as vaccine-induced immune thrombotic thrombocytopenia (VITT). VITT is characterized clinical and laboratory syndromes like: venous (acute cerebral sinus venous thrombosis and abdominal vein thrombosis) or arterial thrombosis; mild-to-severe thrombocytopenia; positive antiplatelet factor 4 (PF4)-polyanion antibodies or anti-PF4–heparin antibodies detected by ELISA; occurring 5–30 days after ChAdOx1 nCoV-19 (AstraZeneca) or Ad26. COV2.S (Johnson & Johnson/Janssen) vaccination and elevated D-dimer. From a pathophysiological point of view, VITT is an autoimmune disease characterized by the development of antibodies that directly activate platelets, causing thrombosis in the arterial or venous systems of the body. At the same time, the components of the vaccine serve as an antigen for the formation of autoantibodies, which enhance the production of platelet factor PF4, which contributes to the formation of blood clots. It has established that intravenous use of immunoglobulin at a dose of 1 g/kg of the patient’s body weight per day, in addition to neutralizing antibodies, makes it possible to suppress VITT-mediated platelet activation. Fondaparinux, direct oral anticoagulants (DOACs), danaparoid or argatroban are the main anticoagulant drugs effective in the treatment of thrombotic conditions in VITT.