Circulating levels of LEVS appear to be increased in adults with chronic B-cell lymphoproliferations (chronic lymphocytic leukemia, small cell lymphoma and mantle cell lymphoma) [91] and [152] and in children with B-cell neoplasm [153]. Finally, LEVS derived from leukemic cells probably play a pathological role by participating to the coagulopathy that is sometimes observed in patients with acute myeloblastic leukemia [154] and [155]. In a study evaluating patients with acute promyelocytic

leukemia (a situation characterized by serious bleeding and thrombotic complications), Ma et al. analyzed LEVS from 30 patients and healthy controls [156]. The morphology of the LEVS was examined by using transmission electron microscopy and laser scanning confocal microscopy. LEVS were quantified and analyzed for their thrombin-generating potential. Counts GSK2118436 concentration of LEVS in patients with acute promyelocitic leukemia were elevated and were typically from promyelocytic cells (CD33+, tissue factor+). The CD33+ LEVS levels correlated with patient leukocyte counts and coagulation activation (evaluated by measuring selleck chemicals d-dimer). Moreover, LEVS from patients decreased the coagulation times and induced thrombin generation; interestingly, LEVS-associated thrombin generation was reduced by adding an anti-human

tissue factor antibody, but neither with anti-factor XI nor anti-tissue factor pathway inhibitor. Vascular homeostasis is the reflection of quiescent, but competent endothelium. EEVS are released by endothelium [157] and [158]. They are now recognized as key players

in a multitude of biological functions necessary for the maintenance of endothelial integrity and vascular biology. EEVS have been demonstrated to act as primary and secondary messengers of vascular inflammation, thrombosis, vasomotor response, angiogenesis, and endothelial survival. EEVS also induce cell cycle arrest through redox-sensitive processes in endothelial cells, thus having implications in vascular senescence [159]. These often-neglected EEVS are emerging as potentially useful indicators of dysfunctioning endothelium. They have been implicated in many different diseases such as pre-eclampsia P-type ATPase in pregnancy [160], pulmonary hypertension [161], chronic graft versus host disease [162], antiphospholipid syndrome [163], or vasculitis such as in Kawasaki’s syndrome [164]. They also have been detected in cancer patients in whose circulating levels of MPS correlate with prognosis, and could be used as prognostic markers for example in advanced non-small cell lung cancer [165]. Very recently, EEVS have been implicated as player in mitral valve disease. In a study of patients with mitral valve disease, Ci et al.