| Literature DB >> 35350251 |
Mohammad Bahadoram1, Ali Saeedi-Boroujeni2, Mohammad-Reza Mahmoudian-Sani1, Helai Hussaini3, Shakiba Hassanzadeh1.
Abstract
Following the outbreak of the COVID-19 pandemic, millions of people around the world have been affected with SARS-CoV-2 infection. In addition to the typical symptoms, thrombotic events, lymphopenia, and thrombocytopenia have been reported in COVID-19 patients. Immune thrombocytopenic purpura (ITP) is one of the thrombotic events that occur in some COVID-19 patients. Hyperinflammation, cytokine storms, and immune dysregulation in some patients are the cause to the main COVID-19 complications such as ALI (acute lung injury), acute respiratory distress syndrome (ARDS), and multiple organ failure. Disruption in the differentiation of T-cells, enhanced differentiation of Th17 and Th1, cell death (pyroptosis), hyper-inflammation and dysfunction of inflammatory neutrophils and macrophages, and hyperactivity of NLRP3-inflammasome are among the important factors that may be the cause to COVID-19-induced ITP. This study aimed to give an overview of the findings on the immunopathogenesis of ITP and COVID-19-induced ITP. Further studies are required to better understand the exact immunopathogenesis and effective treatments for ITP, especially in inflammatory disorders.Entities:
Keywords: COVID-19; SARS-CoV-2; immune dysregulation; immune thrombocytopenic purpura; inflammasome; platelets
Year: 2022 PMID: 35350251 PMCID: PMC8929732 DOI: 10.53854/liim-3001-5
Source DB: PubMed Journal: Infez Med ISSN: 1124-9390