BACKGROUND: The wide diffusion of multicomponent collection in donor apheresis has led to the yielding of different components, such as plasma‐reduced platelet‐pheresis at high PLT concentration. We investigated whether this collection modality could induce more PLT activation compared to standard plateletpheresis.
STUDY DESIGN AND METHODS: Forty‐one plateletpheresis collections (20 Trima and 21 Spectra LRS Turbo v.7.0, COBE) were evaluated. Donor, procedure, and product data were recorded. ADP, collagen, and U46619 (a thromboxane‐A2 analog)‐induced PLT aggregation was investigated in basal (donor) and final (plateletpheresis unit) samples. The expression of PLT activation marker P‐selectin (CD62P) was studied using flow cytometry in basal and final samples. In all cases, P‐selectin was investigated in final samples after stimulation with ADP to assess for a possible further release of the antigen. Four additional plateletpheresis procedures were performed in donors from Group A, using the traditional, nonplasma‐reduced program.
RESULTS: Plateletpheresis obtained by means of the Trima device showed a lower response to in‐vitro induced PLT aggregation and a higher percentage of P‐selectin‐expressing PLT when compared to products obtained using the Spectra device. Moreover, P‐selectin release after ADP stimulation was reduced in plateletpheresis units obtained using the Trima device. These differences disappeared when a nonplasma‐reduced collection program was used. In‐vivo evaluation did not detect any difference between platelepheresis obtained by means of the two cell separators.
CONCLUSIONS: Plateletpheresis units obtained by means of multicomponent collection show a higher degree of PLT activation compared to traditional plateletpheresis procedures when high‐concentration plasma‐reduced products are collected. Randomized clinical studies are needed to assess the real impact of these findings in terms of in‐vivo efficacy of plasma‐reduced plateletpheresis units.
Circulating endothelial cells (CECs) have been studied in cardiovascular disorders and as a marker of angiogenetic activity; clinical applications are limited by a lack of consensus on their phenotypic identification and quantification. We determined CECs in essential thrombocythemia (ET) patients, to investigate their possible pathogenetic role. We considered CECs as CD146 1 /CD45 2 nucleated cells, detected in peripheral blood from 21 healthy controls and 39 ET patients, performing a combination of pre-enrichment of CD146 1 circulating cells and multiparametric flow cytometry measurement (FCM). Levels of CECs in ET patients were higher with respect to controls (median 2844 CECs/mL vs. 121.3 CECs/ mL, P < 0.0001). Apparently hydroxyurea treatment did not influence the levels of CECs. As another established marker of endothelial activation, we also assessed soluble E-selectin (sE-selectin) levels in 31 of the ET patients and compared with 39 healthy volunteers: median sE-selectin level in ET patients was 35.3 ng/mL, higher with respect to controls (24.48 ng/mL), P 5 0.0369. Our data suggest that endothelium in ET is activated, reflecting a significant role of angiogenesis in this disorder and suggesting an important endothelial contribution in the hypercoagulable state of ET patients.
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