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Antibody-induced procoagulant platelets in severe COVID-19 infection #MMPMID33512415
Althaus K; Marini I; Zlamal J; Pelzl L; Singh A; Haberle H; Mehrlander M; Hammer S; Schulze H; Bitzer M; Malek N; Rath D; Bosmuller H; Nieswandt B; Gawaz M; Bakchoul T; Rosenberger P
Blood 2021[Feb]; 137 (8): 1061-1071 PMID33512415show ga
The pathophysiology of COVID-19-associated thrombosis seems to be multifactorial. We hypothesized that COVID-19 is accompanied by procoagulant platelets with subsequent alteration of the coagulation system. We investigated depolarization of mitochondrial inner transmembrane potential (DeltaPsim), cytosolic calcium (Ca2+) concentration, and phosphatidylserine (PS) externalization. Platelets from COVID-19 patients in the intensive care unit (ICU; n = 21) showed higher DeltaPsim depolarization, cytosolic Ca2+, and PS externalization compared with healthy controls (n = 18) and non-ICU COVID-19 patients (n = 4). Moreover, significant higher cytosolic Ca2+ and PS were observed compared with a septic ICU control group (ICU control; n = 5). In the ICU control group, cytosolic Ca2+ and PS externalization were comparable with healthy controls, with an increase in DeltaPsim depolarization. Sera from COVID-19 patients in the ICU induced a significant increase in apoptosis markers (DeltaPsim depolarization, cytosolic Ca2+, and PS externalization) compared with healthy volunteers and septic ICU controls. Interestingly, immunoglobulin G fractions from COVID-19 patients induced an Fcgamma receptor IIA-dependent platelet apoptosis (DeltaPsim depolarization, cytosolic Ca2+, and PS externalization). Enhanced PS externalization in platelets from COVID-19 patients in the ICU was associated with increased sequential organ failure assessment score (r = 0.5635) and D-dimer (r = 0.4473). Most importantly, patients with thrombosis had significantly higher PS externalization compared with those without. The strong correlations between markers for apoptosic and procoagulant platelets and D-dimer levels, as well as the incidence of thrombosis, may indicate that antibody-mediated procoagulant platelets potentially contributes to sustained increased thromboembolic risk in ICU COVID-19 patients.
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Blood 2021 ; 137 (8): 1061-1071
