Pathogenesis of hypoxemia.

Abstract

Thrombocytosis and morphological changes in shape and size of circulating platelets are commonly found in splenectomized thalassemia patients. Functional abnormalities of the platelets are evidently related to their fragile nature. Spontaneous aggregation of platelets can easily occur following application of mild pressure either from a stirring magnetic bar or due to centrifugal force. Platelets are hyper-reactive to chemical stimulation and the release of platelet granule contents (eg ATP) together with other membranous lipid metabolites, thromboxane A2 and malondialdehyde is markedly enhanced. The lipid soluble antioxidant, vitamin E is depleted from various blood compartments. The findings suggest that circulating platelets in splenectomized thalassemia are continuously attacked by yet to be identified blood borne factor(s) and the defective platelets could play a pivotal role in the pathogenesis of hypoxemia.