fibrin has been researched along with Purpura--Thrombocytopenic--Idiopathic* in 3 studies
3 other study(ies) available for fibrin and Purpura--Thrombocytopenic--Idiopathic
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Ultrastructural findings of lung injury due to Vaccine-induced Immune Thrombotic Thrombo- cytopenia (VITT) following COVID-19 vaccination: a scanning electron microscopic study.
Vaccine-induced immune thrombotic thrombocytopenia (VITT) is a rare new syndrome occurring after the ChAdOx1 nCoV-19 vaccine immunization. Patients with VITT are characterized by a variable clinical presentation, likewise also the outcome of these patients is very variable. Here we report the lung ultrastructural findings in the course of VITT of a 58-year-old male patient. Alveoli were mainly dilated, irregular in shape, and occupied by a reticular network of fibrin, while interalveolar septa appeared thickened. The proliferation of small capillaries gave rise to plexiform structures and pulmonary capillary hemangiomatosis-like features. Near the alveoli occupied by a dense fibrin network, the medium-sized arteries showed a modified wall and an intraluminal thrombus. This scenario looks quite similar to that found during COVID-19, where the lungs suffer from the attack of the antigen-antibodies complexes and the virus respectively. In both diseases, the final outcome is a severe inflammation, activation of the haemostatic system and fibrinolysis. Topics: ChAdOx1 nCoV-19; COVID-19; Fibrin; Humans; Lung Injury; Male; Microscopy, Electron, Scanning; Middle Aged; Parenchymal Tissue; Purpura, Thrombocytopenic, Idiopathic; Vaccination | 2022 |
The deglycosylated form of 1E12 inhibits platelet activation and prothrombotic effects induced by VITT antibodies.
In order to improve the safety of COVID-19 vaccines, there is an urgent need to unravel the pathogenesis of vaccineinduced immune thrombotic thrombocytopenia (VITT), a severe complication of recombinant adenoviral vector vaccines used to prevent COVID-19, and likely due to anti-platelet factor 4 (PF4) IgG antibodies. In this study, we demonstrated that 1E12, a chimeric anti-PF4 antibody with a human Fc fragment, fully mimics the effects of human VITT antibodies, as it activates platelets to a similar level in the presence of platelet factor 4 (PF4). Incubated with neutrophils, platelets and PF4, 1E12 also strongly induces NETosis, and in a microfluidic model of whole blood thrombosis, it triggers the formation of large platelet/leukocyte thrombi containing fibrin(ogen). In addition, a deglycosylated form of 1E12 (DG-1E12), which still binds PF4 but no longer interacts with Fcγ receptors, inhibits platelet, granulocyte and clotting activation induced by human anti-PF4 VITT antibodies. This strongly supports that 1E12 and VITT antibodies recognize overlapping epitopes on PF4. In conclusion, 1E12 is a potentially important tool to study the pathophysiology of VITT, and for establishing mouse models. On the other hand, DG-1E12 may help the development of a new drug that specifically neutralizes the pathogenic effect of autoimmune anti-PF4 antibodies, such as those associated with VITT. Topics: Animals; COVID-19; COVID-19 Vaccines; Epitopes; Fibrin; Humans; Immunoglobulin Fc Fragments; Immunoglobulin G; Mice; Platelet Activation; Platelet Factor 4; Purpura, Thrombocytopenic, Idiopathic; Receptors, IgG; Thrombocytopenia; Thrombosis | 2022 |
[The activation of thrombocytogenesis by fibrinogen; unexpected pathogenesis of Werlhof's idiopathic thrombopenia].
Topics: Blood Platelets; Fibrin; Fibrinogen; Humans; Purpura; Purpura, Thrombocytopenic; Purpura, Thrombocytopenic, Idiopathic; Thrombocytopenia | 1951 |