<p>Coagulation Disorders in COVID-19: Role of Toll-like Receptors</p>

Abstract

Coronavirus disease 2019 (COVID-19) has spread rapidly throughout the world. The range of the disease is broad but among hospitalized patients with COVID-19 are coagulation disorders, pneumonia, respiratory failure, and acute respiratory distress syndrome (ARDS). The excess production of early response proinflammatory cytokines results in what has been described as a cytokine storm, leading to an increased risk of thrombosis, inflammations, vascular hyperpermeability, multi-organ failure, and eventually death over time. As the pandemic is spreading and the whole picture is not yet clear, we highlight the importance of coagulation disorders in COVID-19 infected subjects and summarize it. COVID-19 infection could induce coagulation disorders leading to clot formation as well as pulmonary embolism with detrimental effects in patient recovery and survival. Coagulation and inflammation are closely related. In this review, we try to establish an association between virus infections associated with innate immune activation, inflammation and coagulation activation.

Strategies to DAMPen COVID-19-mediated lung and systemic inflammation and vascular injury

“…are closely related to innate immune activation and inflammation, with a strong influence of Toll-like receptors. 39 Currently, the role of anticoagulant therapies in COVID disease is speculative and under investigation although patients with elevated D Dimer or confirmed clots appear to benefit from systemic anticoagulation. Despite the critical importance for risk of thrombotic complications and the contribution to COVID-19 morbidity and mortality, there are no FDA-approved therapies that directly address endothelial cell dysregulation associated with increased coagulation/thrombosis in COVID and non-COVID ARDS.…”

Coagulative Disorders in Critically Ill COVID-19 Patients with Acute Distress Respiratory Syndrome: A Critical Review

“…SARS-CoV-2 may also downregulate angiotensin-converting enzyme 2 (ACE-2) expression, thus regulating overproduction of angiotensin II and concomitant enhancement of IL-6. IL-6 in a positive inflammatory feedback loop inactivates ACE-2, enhancing angiotensin II retention and leading to endothelial activation and inflammation [ 11 ].…”

Potential COVID‐19 Therapeutic Agents and Vaccines: An Evidence‐Based Review

“…The activation of toll‐like receptors, which are expressed in the various innate immune cells, was also indicated to be responsible in COVID‐19–induced coagulopathy. It is noteworthy that increased levels of inflammatory factors, including IL‐6, C‐reactive protein (CRP), lactate dehydrogenase (LDH), and ferritin, along with the procoagulant biomarkers such as fibrinogen and d ‐dimers, are interrelated with a higher mortality rate 18–20 …”