In patients with idiopathic venous thrombosis, interleukin-10 is decreased and related to endothelial dysfunction

被引:43
作者
Poredos, Pavel [1 ]
Jezovnik, Mateja Kaja [1 ]
机构
[1] Univ Med Ctr Ljubljana, Dept Vasc Dis, Ljubljana 1000, Slovenia
关键词
Endothelial dysfunction; Markers of inflammation; Interleukins; Venous thrombosis; CORONARY-ARTERY-DISEASE; BRACHIAL-ARTERY; INFLAMMATORY CYTOKINES; PROCOAGULANT ACTIVITY; THROMBOEMBOLISM; RISK; VASOREACTIVITY; IL-10; CELLS;
D O I
10.1007/s00380-010-0111-3
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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.
引用
收藏
页码:596 / 602
页数:7
相关论文
共 27 条
[1]   Risk factors for venous thromboembolism [J].
Anderson, FA ;
Spencer, FA .
CIRCULATION, 2003, 107 :I9-I16
[2]   On the combined effect of statins and lycopene on cytokine production by human peripheral blood cells [J].
Bergman, Michael ;
Djaldetti, Meir ;
Salman, Hertzel ;
Bessler, Hanna .
HEART AND VESSELS, 2010, 25 (05) :426-431
[3]   Inflammatory cytokines impair endothelium-dependent dilatation in human veins in vivo [J].
Bhagat, K ;
Vallance, P .
CIRCULATION, 1997, 96 (09) :3042-3047
[4]   Noninvasive detection of atherosclerosis [J].
Celermajer, DS .
NEW ENGLAND JOURNAL OF MEDICINE, 1998, 339 (27) :2014-2015
[5]   Inflammatory cytokines as risk factors for a first venous thrombosis:: A prospective population-based study [J].
Christiansen, Sverre C. ;
Naess, Inger Anne ;
Cannegieter, Suzanne C. ;
Hammerstrom, Jens ;
Rosendaal, Frits R. ;
Reitsma, Pieter H. .
PLOS MEDICINE, 2006, 3 (08) :1414-1419
[6]   Chronic systemic inflammation accompanies impaired ventricular diastolic function, detected by Doppler imaging, in patients with newly diagnosed systolic heart failure (Hellenic Heart Failure Study) [J].
Chrysohoou, Christina ;
Pitsavos, Christos ;
Barbetseas, John ;
Kotroyiannis, Iason ;
Brili, Stella ;
Vasiliadou, Karmen ;
Papadimitriou, Lambros ;
Stefanadis, Christodoulos .
HEART AND VESSELS, 2009, 24 (01) :22-26
[7]   The extended IL-10 superfamily: IL-10, IL-19, IL-20, IL-22, IL-24, IL-26, IL-28, and IL-29 [J].
Commins, Scott ;
Steinke, John W. ;
Borish, Larry .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2008, 121 (05) :1108-1111
[8]  
Conde I, 2005, J Thromb Haemost, V3, P2573, DOI 10.1111/j.1538-7836.2005.01660.x
[9]   Guidelines for the ultrasound assessment of endothelial-dependent flow-mediated vasodilation of the brachial artery - A report of the International Brachial Artery Reactivity Task Force [J].
Corretti, MC ;
Anderson, TJ ;
Benjamin, EJ ;
Celermajer, D ;
Charbonneau, F ;
Creager, MA ;
Deanfield, J ;
Drexler, H ;
Gerhard-Herman, M ;
Herrington, D ;
Vallance, P ;
Vita, J ;
Vogel, R .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2002, 39 (02) :257-265
[10]   TH1 AND TH2 T-HELPER CELLS EXERT OPPOSITE REGULATORY EFFECTS ON PROCOAGULANT ACTIVITY AND TISSUE FACTOR PRODUCTION BY HUMAN MONOCYTES [J].
DELPRETE, G ;
DECARLI, M ;
LAMMEL, RM ;
DELIOS, MM ;
DANIEL, KC ;
GIUSTI, B ;
ABBATE, R ;
ROMAGNANI, S .
BLOOD, 1995, 86 (01) :250-257