Modification of platelet shape change parameter by oxidized lipoprotein from beta-thalassemia/Hemoglobin E

Beta-thalassemia/Hemoglobin E (beta-thal/Hb E) is a congenital hemolytic anemia that is prevalent in Thailand Pulmonary arterial occlusion is the cause of morbidity and mortality in these patients. Abnormality of platelets has been implicated as pathogenesis of this condition. However the blood-borne factors that induce platelet activation are not identified Recently, oxidized low-density lipoproteins (ox-LDLs) had been identified in thalassemic blood.

Identify whether oxidized LDL is the blood bone factor that induce platelet activation in beta-thal/Hb E patients.

Platelet activation was measured by monitoring platelet shape change parameter using plasma-free human platelets. The shape change parameter was monitored following exposure to normal LDL, oxidized LDL, and thalassemic LDL.

Oxidized LDL, but not the native LDL and thalassemic LDL, showed platelet activation activity. Oxidation of thalassemic LDL with copper give rise to oxidized LDL with platelet activating activity. However less copper was needed by LDL from splenectomized beta-thal/Hb E patients than those from nonsplencectomized beta-thal/Hb E patients.

LDL from splenectomized beta-thal/Hb E patients is more susceptible for oxidation and gives rise to oxidized-LDL that plays an important role in thrombosis event in these patients.