Increased circulating platelet-leukocyte aggregates in myeloproliferative disorders is correlated to previous thrombosis, platelet activation and platelet count

Platelet-leukocyte adhesion may occur as a consequence of platelet activati on and possibly plays a key role in the deposition of activated platelets a nd fibrin in the thrombotic plug. The aim of the present study was to asses s by whole blood low cytometry the presence of circulating platelet-leukocy te aggregates (PLA) and the platelet-leukocyte response to platelet agonist stimulation (ADP and TRAP) in 50 patients with chronic myeloproliferative disorders (MPD) and 30 controls. PLA were identified as platelet-granulocyt e/monocyte aggregates (PGMA), platelet monocyte aggregates (PMA) and define d as the percentage of leukocytes coexpressing the platelet-specific marker glycoprotein Ib, Compared to controls the mean percentage of PC-MA and PMA was increased in unstimulated whole blood from patients with MPD (7.98 vs. 1.76%; p <0.001 and 12.34 vs. 3.2%; p <0.001, respectively). The percentag e of PGMA was correlated to the platelet count (r = 0.46; p <0.001), percen tage of P-selectin (r = 0.69; p < 0.001) and thrombospondin (r=0.58 I p <0. 001) positive platelets and platelet expression of GPIV (r = 0.33; p = 0.02 ). The mean percentage of PGMA and PMA was significantly increased in ADP-s timulated whole blood of patients (57.14 vs. 47.92%; p=0.009 and 54.91 vs. 45.89%; p <0.001, respectively). Compared to patients without a history of thrombosis, patients having experienced microvascular disturbances or a thr ombotic event had a higher mean percentage of PCMA and PMA in nonstimulated whole blood (10.07 vs. 6.34%; p = 0.025 and 14.81 vs. 10.48%; p=0.021, res pectively) and a higher percentage of PGMA in ADP stimulated whole blood (6 4.32 vs. 51.50%; p < 0.01). These data document an increased frequency of P LA in non-stimulated whole blood in MPD associated with a previous history of thrombosis or microvascular disturbances.