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Studies have also found correlations between the levels of PS externalized on the RBC membrane and plasma levels of hemostatic markers, including prothrombin fragment F1.2, the thrombin–antithrombin complex, the plasmin–antiplasmin complex, and D-dimer, suggesting that increased PS exposure may cause a pathologic RBC procoagulant phenotype, a factor that can induce a hypercoagulable state [107]

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