COVID-19 is Associated with an Acquired Factor XIII Deficiency
Fien A. von Meijenfeldt, Sebastian Havervall, Jelle Adelmeijer, Annika Lundström, Maria Magnusson, Nigel Mackman, Charlotte Thålin, Ton Lisman
Abstract
Coronavirus disease 2019 (COVID-19) is associated with an increased risk of thrombotic complications.[1] Multiple lines of evidence support the existence of a hypercoagulable state in hospitalized COVID-19 patients. Enhanced platelet activation,[2] enhanced in vivo thrombin generation and ex vivo thrombin-generating capacity,[3] [4] hyperfibrinogenaemia,[5] and ex vivo resistance to fibrinolysis[3] [4] [6] [7] have all been demonstrated. Despite a marked ex vivo hypofibrinolytic state, erroneously referred to as 'fibrinolytic shutdown' by some researchers, patients with COVID-19 demonstrate fibrinolytic activity in vivo, as evidenced by elevated plasma levels of plasmin–antiplasmin complexes, and high plasma levels of D-dimer.[3] The hypercoagulable state in COVID-19 persists even in the presence of anticoagulant therapy, as evidenced by elevated plasma levels of thrombin–antithrombin complexes and by ex vivo whole blood viscoelastic tests.[3] [5] [8] Nevertheless, patients with COVID-19 on anticoagulant therapy may experience both bleeding and thrombotic complications.[9]