covid -19诱导的免疫性血小板减少性紫癜;免疫发病机制及临床意义。

M. Bahadoram, A. Saeedi-Boroujeni, M. Mahmoudian-sani, Helai Hussaini, S. Hassanzadeh
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引用次数: 3

摘要

COVID-19大流行爆发后,全球数百万人感染了SARS-CoV-2。除了典型症状外,在COVID-19患者中还报告了血栓形成事件、淋巴细胞减少和血小板减少。免疫性血小板减少性紫癜(ITP)是部分COVID-19患者发生的血栓性事件之一。部分患者的过度炎症、细胞因子风暴和免疫失调是导致急性肺损伤(ALI)、急性呼吸窘迫综合征(ARDS)和多器官衰竭等COVID-19主要并发症的原因。t细胞分化受阻、Th17和Th1分化增强、细胞死亡(焦亡)、炎症中性粒细胞和巨噬细胞的高炎症和功能障碍、nlrp3炎性小体的高活性可能是导致新冠病毒诱导ITP的重要因素。本文就ITP的免疫发病机制及新冠病毒诱导ITP的研究进展进行综述。需要进一步的研究来更好地了解ITP的确切免疫发病机制和有效的治疗方法,特别是在炎症性疾病中。
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COVID-19-induced immune thrombocytopenic purpura; Immunopathogenesis and clinical implications.
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.
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