Abstract
BackgroundMyeloid cells express microparticles that could increase the expression of adhesion molecules including P-selectin. We aimed to evaluate the level of soluble P-selectin (sP-selectin) and prothrombin fragment 1 + 2 (F1 + 2), and to determine correlation of sP-selectin with leukocyte count and F1 + 2 levels in acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) patients.MethodsPatients with newly diagnosed AML (n = 25), CML (n = 13), and controls (n = 17) were recruited in this study. The diagnosis of AML and CML is based on 2001 WHO and/or FAB criteria. Levels of sP-selectin and F1 + 2 were determined using enzyme-linked immunosorbent assay kits (Behring ELISA Processor-III® and Behring Enzygnost F1 + 2).ResultssP-selectin was significantly elevated in CML patients compared to AML patients (p = 0.001). Levels of F1 + 2 in AML and CML patients were significantly increased in comparison to controls (p < 0.001 and p = 0.043). Levels of sP-selectin were significantly correlated to leukocyte count (r = 0.437; p = 0.029) and F1 + 2 (r = 0.436; p = 0.029) in AML patients.ConclusionsAML and CML patients had an increased tendency to thrombosis. While CML patients had higher platelet and/or endothelial activation, hypercoagulable state are more pronounced in AML patients.
Highlights
Myeloid cells express microparticles that could increase the expression of adhesion molecules including P-selectin
A recent meta-analysis reported that venous thromboembolism (VTE) events were highest in chronic myeloid leukemia (CML) patients among other leukemia subtypes [4]
The aim of this study was to investigate levels of sPselectin in myeloid malignancies (AML and CML) patients, and to evaluate its correlation with activation coagulation (F1 + 2) and leukocyte count that specific for hematologic malignancy
Summary
Myeloid cells express microparticles that could increase the expression of adhesion molecules including P-selectin. Malignancies are associated with the development of thromboembolic event, approximately up to six-fold higher than the general population. The pathogenesis of cancer-associated thrombosis (CAT) is multifactorial and complex, mainly related to components of Virchow’s triad [1, 2]. Cancer cells may alter hemostasis by Patients with hematological malignancy carry an increased risk of cancer-associated thrombosis. A recent meta-analysis reported that venous thromboembolism (VTE) events were highest in CML patients among other leukemia subtypes [4]. Circulating microparticles and adhesion molecules play an important role in the mechanism of thrombus formation in hematologic malignancies [5]. P-selectin is expressed on activated platelets and endothelium.
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