Anti-phospholipid syndrome and COVID-19 thrombosis: connecting the dots
| Autor: | Bryce W.Q. Tan, Moon Ley Tung, Robin Cherian, Bharatendu Chandra |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
anti-phospholipid antibodies
Disease Review 030204 cardiovascular system & hematology medicine.disease_cause Autoimmunity 03 medical and health sciences 0302 clinical medicine Rheumatology Antiphospholipid syndrome medicine oxidative stress 030212 general & internal medicine molecular mimicry Endothelial dysfunction anticoagulation thrombosis business.industry autoimmunity COVID-19 medicine.disease Thrombosis Pathophysiology anti-phospholipid syndrome Molecular mimicry Immunology Etiology business AcademicSubjects/MED00010 |
| Zdroj: | Rheumatology Advances in Practice |
| ISSN: | 2514-1775 |
| Popis: | As the coronavirus disease 2019 (COVID-19) pandemic, which is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is spreading rapidly worldwide, it has emerged as a leading cause of mortality, resulting in >1 million deaths over the past 10 months. The pathophysiology of COVID-19 remains unclear, posing a great challenge to the medical management of patients. Recent studies have reported an unusually high prevalence of thromboembolic events in COVID-19 patients, although the mechanism remains elusive. Several studies have reported the presence of aPLs in COVID-19 patients. We have noticed similarities between COVID-19 and APS, which is an autoimmune prothrombotic disease that is often associated with an infective aetiology. Molecular mimicry and endothelial dysfunction could plausibly explain the mechanism of thrombogenesis in acquired APS. In this review, we discuss the clinicopathological similarities between COVID-19 and APS, and the potential role of therapeutic targets based on the anti-phospholipid model for COVID-19 disease. |
| Databáze: | OpenAIRE |
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