Avtor/Urednik		Poredoš, Pavel; Ježovnik, Mateja Kaja
Naslov		In patients with idiopathic venous thrombosis, interleukin-10 is decreased and related to endothelial dysfunction
Tip		članek
Vir		Heart Vessels
Vol. in št.		Letnik 26, št. 6
Leto izdaje		2011
Obseg		str. 596-602
Jezik		eng
Abstrakt		The aim of this study was to evaluate the levels of anti-inflammatory interleukin-10 and pro-inflammatory cytokines and their relationship to endothelial function in patients with idiopathic venous thrombosis. Forty-nine eligible patients of both sexes with idiopathic venous thrombosis and 48 matched control subjects were studied. Levels of inflammatory markers were determined. Endothelial function was evaluated by ultrasound measurement of the flow mediated dilatation (FMD) of the brachial artery. Compared to the control group, patients with idiopathic venous thrombosis had significantly lower levels of interleukin-10 1.81 pg/ml (1.53-2.21) versus 2.71 pg/ml (1.84-3.65), p < 0.001. Patients also had increased levels of pro-inflammatory cytokines: interleukin-6 2.37 pg/ml (1.59-4.09) versus 2.03 pg/ml (1.49-2.59), p = 0.025, interleukin-8 3.53 pg/ml (2.94-5.30) versus 2.25 pg/ml (1.77-2.90), p < 0.001. Furthermore, decreased FMD was observed in patients: 5.0% (3.9-6.9) versus 12.7% (10.8-15.6), p < 0.001. FMD was related to levels of interleukin-10 (r = 0.33, p = 0.001) and was inversely related to pro-inflammatory cytokines interleukin-6 (r = -0.34, p = 0.001) and interleukin-8 (r = -0.43, p < 0.001). Patients with idiopathic venous thrombosis have decreased levels of IL-10 and increased levels of pro-inflammatory cytokines. This imbalance indicates that in the stable phase of the disease, patients have an increased systemic inflammatory response. This inflammatory response could be the consequence of the disease, but most probably is involved in the pathogenesis of venous thrombosis.
Deskriptorji		THROMBOPHLEBITIS INTERLEUKIN-10 ENDOTHELIUM, VASCULAR INFLAMMATION MEDIATORS CYTOKINES BRACHIAL ARTERY VASODILATION INTERLEUKIN-6 INTERLEUKIN-8 TUMOR NECROSIS FACTOR ATHEROSCLEROSIS