“…The increase in platelet volume and the decrease in platelet buoyant density that we observed could be explained by proliferation or dilation of the dense tubular and open canalicular system and reduction of the mitochondria, dense granules, and -granules, as found in ultrastructural studies of platelets from ET patients [25][26][27][28]. Presumably, the origin of the above morphologic findings may be an aberrant proplatelet formation and abnormalities in ploidy, growth rates, and demarcation during the clonal megakaryocytopoiesis of ET, although enhanced platelet activation in the circulation would also be a possibility [2,3,[26][27][28][29][30]. Finally, the high values of MPV and PDW and their correlation with the platelet P-selectin expression suggest that the increased heterogeneity in platelet volume would be related, at least in part, to platelet activation of ET, although no association was observed between the automated platelet parameters and thrombosis.…”