References of the relevant publications were manually screened to avoid missing any eligible studies. of the cases exhibited the primary symptoms within the first two weeks post-vaccination. Headache was the most common initial symptom (>44.2%), and hemorrhage/thrombotic problems (22.46%), as well as discoordination/weakness/numbness/ hemiparesis/cyanotic toes (19.6%), were the most prevalent uncommon initial symptoms. Prothrombin time (PT), D-dimers, and C-reactive protein were the most remarkable increased laboratory parameters in 50.6%, 99.1%, and 55.6% of cases, respectively. In comparison, platelet and fibrinogen were the most remarkable decreased GNE-8505 laboratory parameters in 92.7% and 50.5% of cases, respectively. Most VITT cases presented with cerebral venous thrombosis/cerebral venous sinus thrombosis, supraventricular tachycardia, transverse sinus/cerebral thrombosis, pulmonary embolism, and cerebral hemorrhage. Anti-PF4 antibody measurement through immunoassays and functional assays were positive in 86.2% and 73% of cases, respectively. About 31% of the cases died. Early diagnosis and proper therapeutic measures are important in ChAdOx1 nCov-19 vaccine-induced VITTS patients. Therefore, experts are recommended to know the corresponding clinical and laboratory features, as well as diagnostic methods. Elucidation of the pathophysiologic mechanism of ChAdOx1 nCov-19 vaccine-induced TTS deserves further investigation. Keywords: Cerebral venous sinus thrombosis, Cerebral venous thrombosis, ChAdOx1 nCov-19 vaccine, Oxford AstraZeneca COVID-19 vaccine, Thrombotic thrombocytopenia syndrome Introduction Vaccine-induced thrombotic thrombocytopenia (VITT) GNE-8505 is GNE-8505 usually a severe adverse event upon vaccination associated with extraordinary thrombosis and a concurrent decrease in platelet counts. VITT is likewise known as vaccine-induced prothrombotic immune thrombocytopenia and/or thrombosis with thrombocytopenia syndrome (TTS).1 ChAdOx1 nCoV-19 (Oxford/AstraZeneca) and Janssen COVID-19 vaccines, as adenoviral vector-based vaccines, have been implicated in creating VITT. The probable explanation for such phenomenon TRUNDD is that the free existing DNA in these vaccines might bind to anti-platelet factor 4 (PF4) antibodies.2 VITT is mainly attributed to PF4 antibodies partially like heparin-induced thrombocytopenia (HIT) regarding clinical and biochemical aspects. These immunoglobulin G class antibodies activate platelets via Fc?RIIa receptors, causing them to clump together, leading to clot formation and thrombocytopenia.3 About a hundred cases of thrombosis at atypical sites such as cerebral sinus, splanchnic veins, and the right ventricle with variable degrees of thrombocytopenia have been reported 5 to 30 days upon vaccination with Oxford/AstraZeneca and Janssen COVID-19 vaccines. Microvascular events in the brain, the lungs, and the kidneys have been additionally observed.4 The precise incidence of VITT after vaccination against COVID-19 remains ambiguous due to insufficient clinical experiences, complicated diagnostic methods, several feasibly-involved mechanisms, and lack of well-defined periods for follow-up.5,6 Based on data latest updated in November 2021 offered by Uptodate.com, the highest incidence rates following Oxford/AstraZeneca and Janssen vaccine were 1 in 26?000 and 1 in 533?333, respectively. While crucial risk factors for VITT have not been comprehensively known, young females are proposed as the most vulnerable groups to such an adverse event. Unfortunately, patients with VITT often exhibit intravascular coagulation combined with thrombocytopenia without noticeable clinical symptoms until the immediate onset of thrombosis.7 Infection with SARS-CoV-2 can cause the systemic release of viral RNA leading to activation of the innate immune coagulation pathway associated with systemic and pulmonary immunothrombosis. Recently, COVID-19 viral vectored vaccines such as the ChAdOx1 nCoV-19 vaccine are associated with thrombotic thrombocytopenia after vaccination called VITT.3 One of the main mechanisms clarified by the Greifswald Working Group with Andreas Greinacher leadership was antibody formation against platelet antigens (anti-PF4) due to the stimulation of the immune system and inflammatory reactions. These antibodies can finally lead to an extensive activation of the platelets GNE-8505 via the Fc receptor, which resembles HIT.8 After intramuscular administration of an adenoviral-vectored vaccine, a cascade of events occurs, including microvascular damage, microbleeding and activation GNE-8505 of the platelets with the release of PF4 and disperse of the adenovirus cargo with the engagement of DNA-PF4 can interrupt the immune tolerance causing rare autoimmunity directed by PF4.3 According to the reported deaths associated with ChAdOx1 nCoV-19 post-vaccination VITT, early diagnosis and fast therapeutic measures could benefit the outcome of the patients. In this study, we systematically reviewed the reported cases of post-vaccination thrombotic thrombocytopenia contributed to the ChAdOx1 nCoV-19 vaccine and investigated their laboratory and clinical features and the diagnostic and therapeutic measures applied.