Suppressed networks of inflammatory mediators characterize chronic venous insufficiency.

摘要: Abstract Objective Chronic venous insufficiency (CVI) affects 25 million adults in the United States. Little emphasis has been placed on inflammatory changes associated with CVI. We hypothesize that patients early to mid-stage benign varicose vein disease, differences circulating mediators will be manifested blood draining involved area vs control subjects. Methods Patients undergoing either endovenous ablation or sclerotherapy for Clinical, Etiology, Anatomy, and Pathophysiology clinical class 3 5 disease underwent phlebotomy from regional veins at time of procedure. The patient's age, gender, class, duration symptoms, presence superficial truncal reflux by duplex ultrasound, treatment modality were recorded. Plasma banked samples healthy volunteers (HVs) subjected Luminex (EMD Millipore, Billerica, Mass) evaluate expression an established panel 20 mediators. Mediator concentrations compared between HVs using Mann-Whitney U tests. Importantly, computational analysis allowed us compare not only but also networks connecting these one another. Principal components analyzed assess network robustness each group. Results CVI revealed significantly lower levels monokine induced γ interferon, soluble interleukin (IL) 2 receptor α chain, IL-4, IL-6, IL-7, tumor necrosis factor α, eotaxin, granulocyte-macrophage colony-stimulating than controls. Inflammatory less complex robust HVs. Based principal component analysis, responses among more varied those patients. Conclusions demonstrate have significant blood-borne interconnectedness another their characteristics. suggest hypoinflammation chronic nonhealing These novel findings, if validated larger cohorts, may help predict risk progression response therapy future guide mechanistic studies tissue