Author/Editor		Joras, M; Poredoš, P; Fras, Z
Title		Endothelial dysfunction in Buerger's disease and its relation to markers of inflammation
Type		članek
Source		Eur J Clin Invest
Vol. and No.		Letnik 36
Publication year		2006
Volume		str. 376-82
Language		eng
Abstract		Background Buerger's disease (BD) is a segmental occlusive vascular disease. The aim of this study was to detect functional changes in brachial artery and asytnptomatic morphological changes in extra-cranial carotid arierics not affected by the disease process and to assess markers of inflammation and endothelial damage. Materials and methods Fourteen patients iu the remission phase of BD and the same number of age- and sex-matched healthy controls were included in the study.'Ihe capability of endothelium-dependent (flow-mediated) and endothelium-independent dilation of the brachial artery and intima-media thickness of the carotid arteries were measured using highresolution ultrasound. Laboratory parameters of endogenous fibrinolytic activity, inflammation and endothelial dysfunction were also measured. Results Patients with 13D had a diminished capability of endothelium-dependent vasodilatiou and higher levels of some circulating markers of inflammation, such as leukocytes, C-reactive protein, intcrwllular edhvsion molecule-land li-selecfin. &W ercellular adhesion molecule-I levels were related to some of the inflammatory markers (sedimentation rate, (: reactive protein, a2-globulins and fibrinogen), while f-selectin was correlated with decreased endogenous blood fibrinolytic activity. Endothelium-dependent vasodilation was in negative correlation with the relative share of neutrophil granulocytes. There were no sigrtificant differences in intima-media thickness between patients with BD and controls. Conclusions Our study has expressed generalized lhnctional arterial disorder in patients with BD not accompanied by any measurable morphological changes of the carotid arterial wall. Functional deterioration of brachial artery could be related to increased levels ofvarious inflammatory markers -- the process which is most probahly the basic pathogenetic mechanism of the disease.
Descriptors		THROMBOANGIITIS OBLITERANS ENDOTHELIUM, VASCULAR BRACHIAL ARTERY CAROTID ARTERIES INFLAMMATION MEDIATORS TUNICA INTIMA TUNICA MEDIA BLOOD PRESSURE BLOOD COAGULATION FIBRINOLYSIS