SELP and thalassemia: It is widely accepted that patients with thalassemia have chronically activated platelets, and enhanced platelet aggregation,9 as confirmed by the increased expression of CD62P (P-selectin) and CD63, markers of in vivo platelet activation.10–11 Platelets in thalassemia have a shorter life span, particularly in splenectomized patients, due to enhanced consumption.12 It has also been shown that splenectomized TM and non-splenectomized TI patients have 4 to 10 times more metabolites of prostacyclin (PGI2) and thromboxane A2 (TXA2), both markers of hemostatic activity, than controls.