Abstract
The role of cytokines in the pathogenesis of chronic venous disease (CVD) remains obscure. It has been postulated that oscillatory flow present in incompetent veins causes proinflammatory changes. Our earlier study confirmed this hypothesis. This study is aimed at assessing chemokines and growth factors (GFs) released by lymphocytes in patients with great saphenous vein (GSV) incompetence. In 34 patients exhibiting reflux in GSV, blood was derived from the cubital vein and from the incompetent saphenofemoral junction. In 12 healthy controls, blood was derived from the cubital vein. Lymphocyte culture with and without stimulation by phytohemagglutinin (PHA) was performed. Eotaxin, interleukin 8 (IL-8), macrophage inflammatory protein 1 A and 1B (MIP-1A and MIP-1B), interferon gamma-induced protein (IP-10), monocyte chemoattractant protein-1 (MCP-1), interleukin 5 (IL-5), fibroblast growth factor (FGF), granulocyte colony-stimulating factor (G-CSF), granulocyte-macrophage colony-stimulating factor (GM-CSF), platelet-derived growth factor-BB (PDGF-BB), and vascular endothelial growth factor (VEGF) were assessed in culture supernatants by a Bio-Plex assay. Higher concentrations of eotaxin and G-CSF were revealed in the incompetent GSV, compared with the concentrations in the patients' upper limbs. The concentrations of MIP-1A and MIP-1B were higher in the CVD group while the concentration of VEGF was lower. In the stimulated cultures, the concentration of G-CSF proved higher in the incompetent GSV, as compared with the patients' upper limbs. Between the groups, the concentration of eotaxin was higher in the CVD group, while the IL-5 and MCP-1 concentrations were lower. IL-8, IP-10, FGF, GM-CSF, and PDGF-BB did not reveal any significant differences in concentrations between the samples. These observations suggest that the concentrations of chemokines and GFs are different in the blood of CVD patients. The oscillatory flow present in incompetent veins may play a role in these changes. However, the role of cytokines in CVD requires further study.
Highlights
Chronic venous disease (CVD) affects up to 85% of the population, and more advanced clinical changes (C3–C6 in the Clinical-Etiology-Anatomy-Pathophysiology (CEAP) classification) occur in about 30% of the population [1,2,3,4]
In order to further investigate the role of cytokines released by lymphocytes in CVD, we studied two other panels: chemotactic cytokines and growth factors (GFs)
The CVD group consisted of 34 primary CVD patients with great saphenous vein (GSV) incompetence confirmed by the Doppler ultrasound examination
Summary
Chronic venous disease (CVD) affects up to 85% of the population, and more advanced clinical changes (C3–C6 in the Clinical-Etiology-Anatomy-Pathophysiology (CEAP) classification) occur in about 30% of the population [1,2,3,4]. The impact of inflammatory processes is considered crucial for venous wall remodeling [5,6,7,8,9,10,11]. Reflux in the incompetent veins causes oscillatory flow, with blood moving towards the heart during the contraction of the muscular pump of the calf and backwards during the relaxation of the calf [12]. It has been demonstrated that these flow changes cause the release of proinflammatory cytokines by endothelial cells and lead to leukocyte-mediated inflammatory reactions [12,13,14,15,16]. Our recent publication demonstrated that proinflammatory cytokines are released by lymphocytes in higher concentrations in the incompetent veins [17]
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