Value of Platelet Activation Markers as Prothrombotic Risk Indicators

Lösche, Wolfgang; Heptinstall, Stan

doi:10.1159/000097497

Cited by 9 publications

(12 citation statements)

References 154 publications

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“…the activation status of circulation platelets is less clear. Hyperreactivity of circulating platelets can be characterized by the expression pattern of surface receptors such as P-selectin [ 10 ] and also involves the release of auto- or paracrine activation parameters such as sphingosine-1-phosphat (S1P) [ 10 , 11 ]. S1P is a versatile immunomodulatory lipid mediator which has been implicated in several inflammatory conditions and malignant diseases including GBM [ 11 , 12 ].…”

Section: Introductionmentioning

confidence: 99%

“…The formation of such circulating platelet-immune cell conjugates is considered as a surrogate of inflammatory responses and is well described in diseases such as sepsis and atherosclerosis [ 13 – 16 ]. After in vivo or ex vivo platelet activation, the formation of platelet-leucocyte conjugates (PLC) is typically elevated [ 10 , 16 ].…”

Section: Introductionmentioning

confidence: 99%

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Platelet activation parameters and platelet-leucocyte-conjugate formation in glioblastoma multiforme patients

et al. 2018

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Patients with glioblastoma multiforme (GBM) suffer from an increased incidence of vascular thrombotic events. However, key influencing factors of the primary hemostasis have not been characterized in GBM patients to date. Thus, the present study determines the activation level of circulating platelets in GBM patients, in-vitro reactivity to agonist-induced platelet stimulation and the formation of circulating platelet-leucocyte conjugates as well as the plasma levels of the proinflammatory lipid mediator sphingosine-1-phosphate (S1P). The endogenous thrombin potential (ETP) was determined as global marker for hemostasis.The 21 GBM patients and 21 gender and age matched healthy individuals enrolled in this study did not differ in mean total platelet count. Basal surface expression of platelet CD63 determined by flow cytometry was significantly increased in GBM patients compared to controls as was observed for the concentration of soluble P-selectin in the plasma of GBM patients. While the ETP was not affected, the immunomodulatory lipid S1P was significantly decreased in peripheral blood in GBM. Interestingly, monocyte expression of PSGL-1 (CD162) was decreased in GBM patient blood, possibly explaining the rather decreased formation of platelet-monocyte conjugates.Our study reveals an increased CD63 expression and P-selectin expression/ secretion of circulating platelets in GBM patients. In parallel a down-modulated PSGL-1 expression in circulating monocytes and a trend towards a decreased formation of heterotypic platelet-monocyte conjugates in GBM patients was seen. Whether this and the observed decreased plasma level of the immunomodulatory S1P reflects a systemic anti-inflammatory status needs to be addressed in future studies.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Platelet activation parameters and platelet-leucocyte-conjugate formation in glioblastoma multiforme patients

et al. 2018

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“…White blood cell (WBC)-and platelet (PLT)-derived soluble mediators in PLT concentrates (PCs) are involved in adverse events after PLT transfusion [1][2][3][4] and have been shown to be elevated in clinical conditions that are associated with increased thrombotic risk [5]. Plasma removal [1,2] and prestorage leukoreduction [6][7][8] lower the frequency of febrile non-hemolytic reactions after PLT transfusion, whereas the incidence of allergic reactions has not been altered after the introduction of WBC reduction [6,8], which highlights the role of PLT-derived cytokines.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of White Blood Cell- and Platelet-Derived Cytokine Accumulation in MIRASOL-PRT-Treated Platelets

Picker

Steisel

Gathof³

2009

Transfus Med Hemother

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Background: Soluble mediators in platelet concentrates (PCs) released from contaminating white blood cells (WBCs) and platelets (PLTs) themselves are supposed to promote allergic and non-hemolytic febrile transfusion reactions in the recipient. Pathogen reduction technologies (PRTs) prevent replication and proliferation of pathogens as well as of WBCs, and may reduce cytokine accumulation in PCs during storage and prevent adverse events after PLT transfusion. On the other hand, such treatments may also lead to increased cytokine production by stimulation of WBCs or PLTs due to the photochemical or photodynamical process itself. Material and Methods: 12 triple-dose PLT apheresis collections were leukoreduced by the process-controlled leukoreduction system of the Trima Accel machine and split into 3 units undergoing Mirasol-PRT treatment (M) or gamma irradiation (X) or remaining untreated (C). During storage for up to 7 days, PLT activation, WBC-derived Th-1/2, and inflammatory as well as PLT-derived cytokines were measured by cytometric bead array and enzymelinked immunosorbent assay, respectively. Results: Independent of treatment, all PLT products exhibited low levels of WBC-associated cytokines near or below assay detection limits. WBC-associated cytokines were not elevated by Mirasol-PRT treatment. PLT-derived cytokines were detected at higher levels and increased significantly during storage in all units. Most likely due to higher PLT activation, M units showed significantly higher levels of PLT-derived cytokines compared to untreated and gamma-irradiated units on day 5 of storage. Conclusion: In all PCs, PLTs themselves were the main source of cytokine release. Mirasol-PRT treatment was associated with a significantly increased PLT activation and accumulation of PLT-derived cytokines during storage, without affecting WBC-derived cytokines relative to controls.

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“…Platelet activation markers correlate with intraoperative blood loss, and the use of volatile anaesthetics [13,36,37]. The value of platelet activation markers as indicators for the prothrombotic risk is outlined in a further review of this series [38]. The minimal manipulation required for flow cytometry allows detection of platelet function in the physiologic milieu.…”

Section: Determination and Quantification Of Platelet Activation Markersmentioning

confidence: 99%

Diagnostic Methods for Platelet Function Analysis

Klouche¹

2007

Transfus Med Hemother

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Platelets play a key role in the regulation of haemostasis, clot stability and retraction, vascular repair, and exert an increasingly recognised function in host defence. Conversely, platelets are also implied in many pathophysiological processes, such as thrombosis, haemorrhage, inflammation, atherogenesis, tumour growth and metastasis. Thus quantitative and qualitative platelet alterations have been associated with distinct clinical diseases, including cardiovascular diseases, diabetes, tumour metastasis and sepsis, and consequently different diagnostic platelet markers are correlated with the prognosis and severity of these diseases. While primary platelet functional abnormalities are very rare diseases, acquired platelet function disorders are rather frequent and occur in the context of many diseases and in association with several drugs. Furthermore, the introduction of a great variety of different anti-platelet agents leads to iatrogenic states of therapeutically reduced platelet function. This review provides an overview of the methodological principles of platelet function analysis, the currently available diagnostic devices, the application and suitability for the diagnosis of different platelet function disorders and the restrictions of each method, to promote an optimal selection of diagnostic tests.

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Value of Platelet Activation Markers as Prothrombotic Risk Indicators

Cited by 9 publications

References 154 publications

Platelet activation parameters and platelet-leucocyte-conjugate formation in glioblastoma multiforme patients

Platelet activation parameters and platelet-leucocyte-conjugate formation in glioblastoma multiforme patients

Evaluation of White Blood Cell- and Platelet-Derived Cytokine Accumulation in MIRASOL-PRT-Treated Platelets

Diagnostic Methods for Platelet Function Analysis

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