靶向SARS-CoV-2刺突蛋白单克隆抗体治疗慢性难治性特发性血小板减少性紫癜后的短暂完全恢复

IF 0.7 Q4 HEMATOLOGY
Pooja Gogia, Yiqing Xu
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引用次数: 0

摘要

特发性血小板减少性紫癜(ITP),也称为免疫性血小板减少性紫癜,是一种免疫介导的获得性疾病,其特征是由于自身免疫相关的血小板破坏导致血小板计数短暂或持续减少。ITP的治疗依赖于竞争和抑制自身抗体结合和破坏(静脉注射免疫球蛋白和抗d免疫球蛋白和脾酪氨酸激酶(Syk)抑制剂fostamatinib),增加血小板产生(血小板生成素受体激动剂),免疫抑制以减少自身抗体产生,以及脾切除术。对血小板自身抗原的研究表明,表位主要位于GP IIb/IIIa受体或整合素αIIbβ3上,但ITP发生的触发因素尚不清楚。我们在此报告了一例37岁的慢性ITP患者,他接受了针对SARS-CoV-2的单克隆抗体(mAb),即卡西维单抗和imdevimab治疗他的COVID-19感染后,他的血小板计数在短时间内完全恢复。我们讨论了几种潜在的作用机制,并提出进一步的研究来阐明COVID-19单抗对ITP的治疗作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Transient Complete Recovery of Chronic Refractory Idiopathic Thrombocytopenic Purpura after Treatment with Monoclonal Antibody Targeting SARS-CoV-2 Spike Protein
Idiopathic thrombocytopenic purpura (ITP), also known as immune thrombocytopenic purpura, is an immune-mediated acquired disease characterized by transient or persistent decrease of the platelet count due to autoimmune-related destruction of platelets. Therapy for ITP relies on competing and inhibiting the autoantibody binding and destruction (intravenous immunoglobulin and anti-D immunoglobulin and spleen tyrosine kinase (Syk) inhibitor fostamatinib), augmenting platelet production (thrombopoietin receptor agonists), immunosuppression to reduce the autoantibody production, as well as splenectomy. Studies on autoantigens on the platelets suggested epitopes to be located predominantly on the GP IIb/IIIa receptor or integrin αIIbβ3, though the trigger for the development of ITP is unclear. We report a case here of a 37-year-old gentleman who has chronic ITP managed on eltrombopag, who after receiving monoclonal antibody against SARS-CoV-2 (mAb) i.e. casirivimab and imdevimab for his COVID-19 infection, demonstrated complete recovery of his platelet count for a short period of time. We discuss a few potential mechanisms of action and propose further studies to elucidate the therapeutic effect of COVID-19 mAb in ITP.
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