Abstract
The coronavirus disease 2019 (COVID-19) is a contagious respiratory tract infection caused by the betacoronavirus SARS-CoV-2. The World Health Organization declared the COVID-19 outbreak a pandemic on March 11, 2020. Since the COVID-19 pandemic started, more than 166 million patients have been tested positive worldwide with more than 3.4 million related death recorded. COVID-19 has a wide range of signs and symptoms. Hematological changes such as lymphopenia, thrombocytopenia, and coagulation disturbances are not unusual in patients with COVID-19. However, the mechanisms causing these changes are partially comprehended. Immune thrombocytopenia was identified to be among the hematologic autoimmune diseases seen in patients infected with SARS-CoV-2. This review summarizes the evidence on COVID-19-associated immune thrombocytopenia and the underlying mechanisms involved in its development.
Highlights
The coronavirus disease 2019 (COVID-19) is a contagious respiratory tract infection caused by the beta-coronavirus SARS-CoV-2
This review summarizes the evidence on COVID19-associated immune thrombocytopenia and the underlying mechanisms involved in its development, based on the PubMed database
Since the outbreak of the pandemic, there were several case reports of immunemediated thrombocytopenia linked to COVID-19
Summary
The coronavirus disease 2019 (COVID-19) is a contagious respiratory tract infection caused by the beta-coronavirus SARS-CoV-2. Studies have identified many cases of COVID-19 patients who developed autoimmune events such as antiphospholipid syndrome, autoimmune cytopenia, Guillain-Barré syndrome and Kawasaki disease These results suggest that SARS-CoV-2 infection is linked to the development of autoimmune diseases [11,12]. Zulfiqar et al published the first single case report indicating that COVID-19 infection could be linked to immune thrombocytopenia. He described a case of “de novo” ITP in a 65-year-old woman with COVID-19 who underwent a multi-drug treatment, including intravenous immunoglobulin (IVIG), prednisolone, and eltrombopag, to recover completely [26]. Concerning the management of the documented cases, medications used were: steroids (prednisone, dexamethasone, and methylprednisone), intravenous immunoglobulin (IVIG), thrombopoietin receptor agonists (TPO-RA e.g. Romiplostim and Eltrombopag),
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