While thrombocytosis is expected in the post splenectomy setting, it is not usually associated with thrombotic episodes. However, in this case the combination of hemolysis, thrombocytosis, and HS may have led to a HCS. Previous investigators have established that in the absence of endothelial damage, erythrocytes and endothelial cells do not present sufficient amounts of phosphatidylserine on the cell surface to bind factors X and Xa In vitro, it has been shown that HS cells have
accelerated lipid loss , which may provide increased substrate for procoagulant activation. Furthermore, when
platelets are activated their phosphatidylserine content increases from 13% to approximately 30%. Platelet activation causes the transfer of anionic phospholipid (primarily phosphatidylserine) from the inner to the outer leaflet of the membrane, accelerating the coagulation process
While thrombocytosis is expected in the post splenectomy setting, it is not usually associated with thrombotic episodes. However, in this case the combination of hemolysis, thrombocytosis, and HS may have led to a HCS. Previous investigators have established that in the absence of endothelial damage, erythrocytes and endothelial cells do not present sufficient amounts of phosphatidylserine on the cell surface to bind factors X and Xa In vitro, it has been shown that HS cells have
accelerated lipid loss , which may provide increased substrate for procoagulant activation. Furthermore, when
platelets are activated their phosphatidylserine content increases from 13% to approximately 30%. Platelet activation causes the transfer of anionic phospholipid (primarily phosphatidylserine) from the inner to the outer leaflet of the membrane, accelerating the coagulation process
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