Coagulopathies are common in hematological malignancies and can cause life-threatening bleeding or thrombosis. Extracellular vesicles (EVs), including exosomes, microvesicles, and apoptotic bodies, carry cargo that reflects their cellular origin. They frequently express tissue factor (TF) and expose phosphatidylserine (PS), which initiate and amplify coagulation and can also transport fibrinolytic mediators that modulate plasmin generation. Procoagulant EVs are commonly assessed using TF- and PS-dependent functional assays, global hemostasis tests such av overall hemostatic potential, and flow cytometric phenotyping. Clinical and experimental data show elevated EV numbers and activity at diagnosis in several hematological malignancies. In acute leukemias, EV-associated procoagulant activity often declines with treatment yet may remain above control levels, consistent with residual risk. In plasma cell disorders and myeloproliferative neoplasms, platelet-derived and TF/PS-positive EVs are frequently increased and have been linked to enhanced thrombin generation. EVs appear to play key roles across leukemias, multiple myeloma, lymphoid and myeloproliferative neoplasms. However, considerable methodological heterogeneity, including differences in pre-analytical handling, EV isolation, characterization, and activity measurement limits comparability and clinical translation. Disease-specific mechanistic studies are needed to clarify how EVs modulate hemostasis in different hematologic malignancies. In parallel, standardized protocols and adequately powered clinical studies are required to validate EVs as biomarkers.
Gran et al. (Thu,) studied this question.