Abstract
The current COVID-19 pandemic emerged in December 2019, in China, affecting millions of people worldwide. COVID-19 is mainly a disease of the respiratory system, yet systematic complications have also been reported among SARS-CoV-2 infected patients. Thrombotic complications are one of the severe clinical outcomes of COVID-19, especially among critically ill patients, and are associated with poor prognosis. To date, many studies have concluded that COVID-19 increases the incidence of thrombotic events and coagulopathies; however, the exact mechanism behind such a disease outcome is not well known. Various pathophysiological mechanisms for thrombotic events in COVID-19 have been proposed, these include virus-induced endothelial cell damage, inflammation, and excess production of pro-inflammatory cytokines. As a result, most critically diseased COVID-19 patients are managed with prophylactic anticoagulant, yet some still develop thrombotic episodes. Therefore, better understanding of the mechanisms behind the thrombotic complications is needed to develop treatments that specifically target such pathways, which may aid in better disease management and improve the prognosis.
Highlights
In December 2019, the Chinese Center for Disease Control and Prevention identi fied the presence of a novel coronavirus in throat swab samples from a series of pneumonia cases of unknown etiology, that presented with dry cough, dyspnea, and fever.[1]
Wang et al[19] reported that, among 199 COVID-19 patients, elevated levels of D-dimer, fibrinogen degradation products, prolonged pro thrombin time, and thrombin time were found to be higher among patients with severe disease manifestations. These findings indicate that COVID-19 is associated with abnor mal coagulation and subsequently leads to thrombotic complications and severe disease outcome
Low-molecular-weight heparin is considered more beneficial than other prophylactic regi mens, in COVID-19 cases, as it has been previously reported that it has a longer half-life than unfractionated heparin,[51] acts as an inhibitor for viral attachment by binding to SARS-CoV-2 spike protein,[52] and it has immunomodulatory and anti-inflammatory effects.[53]
Summary
In December 2019, the Chinese Center for Disease Control and Prevention identi fied the presence of a novel coronavirus in throat swab samples from a series of pneumonia cases of unknown etiology, that presented with dry cough, dyspnea, and fever.[1]. These findings indicate that COVID-19 is associated with abnor mal coagulation and subsequently leads to thrombotic complications and severe disease outcome.
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