COVID-19-induced immune thrombocytopenic purpura; Immunopathogenesis and clinical implications

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 COV-ID-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), SUMMARYhyper-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.

The relationship of skin disorders, COVID-19, and the therapeutic potential of ginseng: a review

“…Immune thrombocytopenic purpura (ITP) is an autoimmune disease characterized by platelet destruction [ 55 ]. The pathogenesis of COVID-19-induced ITP is unclear, but the dysregulation of T-cells and hyperactivity of the NLRP3 inflammasome have been suggested as potential causes [ 56 ]. In ITP, Th17 levels are increased, and the unbalanced Th1/Th2 ratio produces autoantibodies against platelets.…”

“…The elevation of Th17 and plasma IL-17 levels have been reported in patients with COVID-19 and stimulates keratinocytes, fibroblasts, neutrophils, and endothelial cells while promoting tissue inflammation [ 57 , 58 ]. Additionally, inflammasome activation leads to the production of cytokines such as IL-1β and IL-18, and the overactivation of IL-18 can accelerate the proliferation and cytotoxicity of CD8+ T cells [ 56 ].…”

Recommendations on the Management of Patients with Immune Thrombocytopenia (ITP) in the Context of SARS-CoV-2 Infection and Vaccination: Consensus Guidelines from a Spanish ITP Expert Group

“…The use of rituximab is not recommended, since it can decrease the formation of antibodies against SARS-CoV-2 virus. In this sense, the use of immunosuppressants is discouraged unless there is no adequate therapeutic option, although it should be assessed individually [ 20 ].…”