Abstract
Circulating endothelial cells (CECs) are viable, apoptotic or necrotic cells, identified by CD 146 surface antigen expression, considered a biomarker of thrombotic risk, given their active role in inflammatory, procoagulant and immune processes of the vascular compartment. Growing evidence establishes that CECs are also involved in the pathogenesis of several hematological and solid malignancies. The primary aim of this study was to verify if CEC levels could predict both the course and treatment responses of splanchnic vein thrombosis (SVT), either in patients affected by myeloproliferative neoplasms (MPNs) or liver disease. Thus, a retrospective multicenter study was performed; fifteen patients receiving anticoagulant oral treatment with vitamin k antagonists (VKA) for SVT were evaluated. Nine patients were affected by MPN, and all of them received cytoreduction in addition to anticoagulant therapy; four of these patients had primary myelofibrosis (PMF) and were treated with ruxolitinib (RUX), and one patient with primary myelofibrosis, two patients with essential thrombocythemia (ET), and two patients with polycythemia vera (PV) were treated with hydroxyurea (HU). Six patients affected by liver diseases (three with liver cirrhosis and three with hepatocellular carcinoma) were included as the control group. CECs were assayed by flow cytometry on peripheral blood at specific time points, for up to six months after enrollment. The CEC levels were related to C-reactive protein (CRP) levels, splenic volume reduction, and thrombus recanalization, mainly in MPN patients. In patients with liver cirrhosis (LC) and hepatocellular carcinoma (HCC), for which the mechanism of SVT development is quite different, the relationship between CEC and SV reduction was absent. In conclusion, the CEC levels showed a significant correlation with the extent of venous thrombosis and endothelial cell damage in myeloproliferative neoplasm patients with splanchnic vein thrombosis. Although preliminary, these results show how monitoring CEC levels during cytoreductive and anticoagulant treatments may be useful to improve SVT outcome in MPN patients.
Highlights
Circulating endothelial cells (CECs) are a specific population of endothelial cells, identified by CD146 surface antigen expression, using flow cytometry; CECs are usually present at a very low percentage in the peripheral blood (0.01% of the mononuclear cells) [1].CECs are involved in angiogenesis, but they actively take part in inflammatory, procoagulant and immune processes of the vascular compartment, in equilibrium with vessel endothelial cells [2]
Growing evidence suggests that CECs play an important role in the pathogenesis of several hematological diseases; high levels of mature, resting, activated circulating endothelial cells and CECs have been observed within the course of both solid and hematological neoplasms [4–9]
The CEC levels are directly related to C-reactive protein (CRP) in all three treatment groups (r = 0.7 in group A, r = 0.9 in group B, and r = 0.9 in group C)
Summary
CECs are involved in angiogenesis, but they actively take part in inflammatory, procoagulant and immune processes of the vascular compartment, in equilibrium with vessel endothelial cells [2]. Given their role in inducing the expression of proinflammatory signals by endothelial cells, CECs may be considered as biomarkers of vascular injury and thrombotic risk [3]. With special regard to myeloproliferative neoplasms (MPNs), an increased CEC count may reveal endothelial damage in patients with VTE, and express different endothelial activation phenotypes, depending on the disease state. In a subgroup of subjects with acute DVT, the CEC levels progressively decreased within 9–15 months after the acute event [10]
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