A team of researchers from the USA and Sweden has recently demonstrated that increased levels of the proinflammatory cytokine, angiopoietin-2 (ANG2), is responsible for hypercoagulation observed in severe COVID-19 patients. In the current study, the scientists evaluated whether an elevated plasma level of ANG2 in critically ill COVID-19 patients can modulate the coagulation system by inhibiting thrombomodulin-mediated activation of protein C.
The study was conducted on 20 critically ill COVID-19 patients admitted to the ICU for more than 10 days. Overall, an elevated ANG2 level was observed in plasma samples of all critically ill COVID-19 patients. A significantly high ANG2 level was found to be associated with the risk of organ failure and death. Significantly elevated levels of platelet, D-dimer, and von Willebrand factor and significantly reduced levels of ADAMTS13 were observed in all COVID-19 patients. ANG2 was found to inversely correlate with the ADAMTS13 level. These observations indicate that the pro-coagulation process is significantly impaired in these patients and that ANG2 plays a crucial role in mediating hypercoagulation, which is a frequently observed symptom in critically ill COVID-19 patients.
The study findings demonstrate that an increased level of ANG2, a proinflammatory cytokine, in COVID-19 patients is associated with disease severity, hypercoagulation, and mortality. Given these observations, the scientists believe that therapeutic inhibition of ANG2 can be a potential approach for treating severe COVID-19 patients, as well as for alleviating cardiovascular complications associated with the disease.
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