Abstract Number: PB1793
Meeting: ISTH 2020 Congress
Background: Among all chronic myeloproliferative neoplasms, platelet hemostatic abnormalities in primary myelofibrosis (PMF) have been the least studied. Despite strong evidence of in vivo platelet activation, patients with PMF may present an increased incidence of thrombosis as well as bleeding complications. Nevertheless, the treatment options include aspirin alone as primary prevention for the low-risk patients, and specific therapy combined with aspirin for the other patients.
Aims: The aim of our study was to evaluate the platelet function in patients with PMF.
Methods: Light transmission aggregometry was utilized to characterize the platelet function in 47 patients with PMF and 30 healthy volunteers. 12 patients were treated with ruxolitinib, 5 of them also got an antiplatelet therapy; 35 patients didn’t have a specific therapy, 9 of them got an antiaggregants. Platelet aggregation was induced by adenosine diphosphate (ADP) in two concentrations, collagen and ristocetin.
Results: The maximum aggregation rate (MA, %) of ADP and collagen was significally lower in patients than in controls, the MA of ristocetin was the same in both groups (Table 1, *p < 0.05 compared to controls). But when we compared platelet function in patients with and without specific therapy, we found that the MA of ristocetin was significally lower in patients treated by ruxolitinib (Table 2). Surprisingly, there was no correlation between aggregation patterns and antiplatelet therapy in both groups of patients.
Conclusions: The reduced response to ADP and collagen stimulation in patients with PMF can be a consequence of disease – associated intravascular platelet activation and the pre-term devastation of the platelet granules. The impaired platelet aggregation response to ristocetin may reflect the effect of the specific therapy due to abnormalities in von Willebrand factor – platelet interactions. It could be concluded that the platelet function and antiplatelet therapy regimen in patients with PMF remains unclear and needs further investigation.
|Agonist||Final concentration||Patients, n=47 (Me, 95% CI)||Controls, n=30 (Me, 95% CI)|
|ADP||1 µM/L||8,5 *(2,4 – 26,9)||19,5 (12,1 – 26,6)|
|ADP||5 µM/L||40,0 *(16,6 – 75,7)||54,0 (36,2 – 77,4)|
|Collagen||2 µg/mL||6,2 *(0,7 – 76,3)||53,3 (38,2 – 84,8)|
|Ristocetin||1,2 µg/mL||78,5 (22,1 – 99,2)||73,7 (55,9 – 91,8)|
[Table 1. Aggregation tests in patients with PMF and control group (MA, %).]
|Agonist||Final concentration||Patients with ruxolitinib, n=12 (Me, 95% CI)||Patients without ruxolitinib, n=35 (Me, 95% CI)|
|ADP||1 µM/L||11,9 (2,3 – 20,3)||8,0 (2,4 – 26,9)|
|ADP||5 µM/L||35,7 (4,4 – 63,5)||42,1 (16,6 – 79,7)|
|Collagen||2 µg/mL||5,0 (0,7 – 54,1)||6,6 (1,5 – 88,4)|
|Ristocetin||1,2 µg/mL||68,5* (9,3 – 92,0)||83,2 (22,9 – 99,4)|
[Table 2. Aggregation tests in patients subject to ruxolitinib taking (MA, %).]
To cite this abstract in AMA style:Smirnova O, Tarkovskaya L, Korsakova N, Silina N, Fominykh M, Voloshin S, Papayan L. Platelet Function in Primary Myelofibrosis [abstract]. Res Pract Thromb Haemost. 2020; 4 (Suppl 1). https://abstracts.isth.org/abstract/platelet-function-in-primary-myelofibrosis/. Accessed September 24, 2023.
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