Essential thrombocythemia (ET) is a Philadelphia-negative myeloproliferative neoplasm with high platelet counts and an increased risk of thrombosis. Acquired somatic mutations delineate four ET subtypes: JAK2-V617F, CALR-mutated, MPL-mutated, and “Triple-Negative”(TN). 1 CALR mutations appear to drive a distinct phenotype, consisting of a higher proportion of males, younger age, higher platelet count, lower hemoglobin level and white cell count and lower thrombotic risk than JAK2-V617F carriers. 1-3 TN patients share the same profile, but lack the higher platelet count. 4 Thrombogenesis in ET results from complex interactions between blood cells and plasma factors. 5 Microparticles (MPs) are thought to play a role in many thrombotic processes. 6 They are sub-micron plasma membrane vesicles, released into the circulation by blood and endothelial cells following activation or apoptosis. 6 They can be labeled with annexin V if phosphatidylserine (PS) is exposed during their formation. 6 So called plateletderived microparticles (PMPs) are the most abundant MP subtype in the blood, and could originate mainly from megakaryocytes. 7

Prior to the discovery of CALR mutations, an increase in PMPs was reported in ET patients as compared to healthy controls8 and hypercoagulability was ascribed, at least in part, to MPs. 9, 10 However, to our knowledge, the patterns of MPs according to mutational status have not