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A Journal on Angiology
Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,899
International Angiology 2010 June;29(3)226-31
Idiopathic venous thrombosis is related to systemic inflammatory response and to increased levels of circulating markers of endothelial dysfunction
Jezovnik M. K. , Poredos P.
Department of Vascular Disease, University Medical Centre Ljubljana, Slovenia
AIM: During the past decade, the role of inflammation in the pathophysiology of arterial thrombosis has been elucidated. However, little is known about the relationship between inflammation and venous thrombosis. Recently, inflammation has been accepted as a possible mechanism through which different risk factors trigger thrombus formation in veins. The aim of the present study was to investigate the inflammatory markers and their relationship to idiopathic venous thrombosis.
METHODS: Fourty-nine patients with first idiopathic venous thrombosis and 48 age matched control subjects were included in the study. Patients were studied 2-4 months after the acute event. Patients and control subjects did not differ in the classical risk factors of atherosclerosis, except in body mass index. In both groups, blood markers of inflammation, namely high sensitive C-reactive protein (hs CRP), interleukins (IL-6, IL-8) and tumour necrosis factor alpha (TNF-a), and circulating markers of endothelial dysfunction/damage namely von Willebrand factor (vWF), P-selectin and the vascular adhesion molecule (VCAM-1) were measured.
RESULTS: In comparison to healthy subjects patients had significantly higher levels of inflammatory markers: hs CRP: 2.58 mg/L (1.37-6.61), vs. 1.67 mg/L (0.97-3.24) P=0.044, IL-6: 2.37 pg/mL (1.59-4.10), vs. 2.03 pg/mL (1.45-2.59), P=0.025, IL-8: 3.53 pg/mL (2.94-5.3), vs. 2.25 pg/mL (1.77-2.90) P≤0.0001. However, concentrations of TNF-a did not differ significantly between the groups. Also in patients higher levels of circulating markers of endothelial dysfunction: vWF 150.0 g/L (121.0-195.0) vs. 91.5 g/L (70.5-104.0), P≤0.0001, P-selectin 39.5 pg/L (34.0-40.6) vs. 34.8 pg/L (32.5-38.6) P=0.009. In contrast, levels of VCAM-1 were comparable between the groups. The levels of some inflammatory markers were related to the concentration of von Willebrand factor and P-selectin - IL-6: vWF (r=0.36, P=0.08), hs CRP: P-selectin (r=0.44, P=0.018), IL-6: P-selectin (r=0.51, P=0.0002), IL-8: P-selectin (r=0.38, P=0.043).
CONCLUSION: Patients with idiopathic venous thrombosis have increased levels of circulating markers of inflammation and blood markers of endothelial dysfunction. Higher levels of both groups of markers indicate that patients in the stable phase of the disease have an increased systemic inflammatory response. The interrelationship between inflammatory markers and markers of endothelial dysfunction favour the hypothesis that inflammation could be involved in the etiopathogenesis of idiopathic venous thrombosis.