COVID-19 concerns aggregate around platelets

Abstract

In this issue of Blood, articles by Manne et al and Hottz et al highlight platelet hyperactivity in COVID-19–associated pathophysiology.^, Although the hallmarks of COVID-19 include a brisk inflammatory response and respiratory symptoms, the hematologic manifestations of this infection have also garnered attention, with thrombotic complications taking center stage.^, COVID-19–associated coagulopathy has been characterized by an elevated D-dimer, mild thrombocytopenia, and a prolongation of the activated partial thromboplastin time. Alongside these laboratory abnormalities, patients present with increased rates of thrombosis. The role of platelets in the thrombotic complications of COVID-19 is explored in these 2 articles, establishing that platelet hyperactivity contributes to the coagulopathy seen in COVID-19.

Schematic cross-section of a blood vessel depicting COVID-19–associated endothelial damage (left panel). At the site of endothelial injury, platelets become activated and aggregate (middle panel). These hyperactive platelets activate monocytes, leading to release of tissue factor, the principle regulator of the coagulation cascade (right panel). RBC, red blood cell.