Background: Some conventional vaccines have been recognized as a cause of secondary immune thrombocytopenia (ITP). According to recent publications, mRNA vaccines are probably associated with an increased risk of ITP.
Case Presentation: Our patient developed severe ITP one week after the second dose of COVID-19 mRNA vaccine. Medical management was not effective, requiring splenectomy to obtain sustained remission.
Conclusion: Considering the temporality and immunological hypothesis, we consider the vaccine to be the trigger of this ITP. To our knowledge, our case is, to date, the most severe case of ITP reported following SARS-CoV-2 vaccination and could help for the therapeutic management of similar patients.
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http://dx.doi.org/10.1186/s12959-022-00404-z | DOI Listing |
J Thromb Haemost
December 2024
Laboratory of Immunopharmacology, Oswaldo Cruz Institute, Oswaldo Cruz Foundation (FIOCRUZ), Rio de Janeiro, Brazil. Electronic address:
Background: Although rare, vaccine-induced thrombotic thrombocytopenia (VITT) following adenoviral vector COVID-19 vaccination is a concerning and often severe adverse effect of vaccination. The generation of high anti-platelet factor 4 (PF4) antibody titers, promotes the formation of immune complexes capable of activating platelets and neutrophils through FcγRIIa.
Objective: Given that Platelet-leukocyte aggregate (PLA) formation and inflammasome activation are common features of thromboinflammatory diseases, we aimed to evaluate if these are also features of VITT.
Vaccine-induced immune thrombotic thrombocytopenia (VITT) is a rare but serious prothrombotic adverse event following vaccination with adenovector-based COVID-19 vaccines. Laboratory findings indicate that anti-platelet factor 4 (PF4) immunoglobulin G antibodies are the causing factor for the onset of thromboembolic events in VITT. However, molecular mechanisms of cellular interactions, signaling pathways and involvement of different cell types in VITT antibody-mediated thrombosis are not fully understood.
View Article and Find Full Text PDFInt J Hematol Oncol Stem Cell Res
October 2024
Department of Immunology, Faculty of Medicine, Lorestan University of Medical Sciences, Khorramabad, Iran.
Human platelet antigens (HPAs) play a clinically significant role in alloimmunization and the development of immune-mediated disorders such as immune thrombocytopenia (ITP), fetal and neonatal alloimmune thrombocytopenia (FNAIT), and post-transfusion purpura (PTP). Understanding the genetic profiles of HPAs is critical for preventing and treating these conditions. Given the limitations of serological methods in determining HPA genotypes, this study aims to investigate the association between the genotypes of HPA1, HPA2, HPA3, HPA4, and HPA15 antigens and autoimmune thrombocytopenia in Lorestan Province, utilizing the PCR-SSP method.
View Article and Find Full Text PDFClin Pharmacol Drug Dev
December 2024
R&D Center, GEROPHARM, Saint-Petersburg, Russia.
During biosimilar drug development, conducting a clinical trial of biosimilar efficacy in patients may become necessary in the presence of residual uncertainty regarding the biosimilarity of the drugs. In the development of the biosimilar romiplostim GP40141, we aimed to use a model-based in silico clinical trial (ISCT) approach to optimize the planned biosimilar efficacy trial in patients with immune thrombocytopenia. The population pharmacokinetic/pharmacodynamic model for healthy volunteers was modified and validated to describe platelet dynamics in patients with immune thrombocytopenia.
View Article and Find Full Text PDFHum Cell
December 2024
Department of Oncology, Donghu District, First Affiliated Hospital of Nanchang University, No. 17 Yongwaizheng Street, Nanchang, 330000, Jiangxi, China.
Immune thrombocytopenia (ITP) is a common hematological disorder. Our previous study has found that exosomal miR-146a-5p derived from bone marrow mesenchymal stromal cells (BMSCs) regulate Th17/Treg balance to alleviate ITP. This work further investigated the role of miR-146a-5p in ITP with pregnancy.
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