Avtor/Urednik		Štalc, Monika
Naslov		Ocenjevanje endotelijske funkcije pri bolnikih z antifosfolipidnim sindromom
Tip		monografija
Kraj izdaje		Ljubljana
Založnik		Medicinska fakulteta
Leto izdaje		2007
Obseg		str. 55
Jezik		slo
Abstrakt		Introduction: Antibody mediated endothelial cell injury has been identified as a factor potentially involved in the pathogenesis of thrombosis in antiphospholipid syndrome. A relationship between antiphospholipid antibodies and endothelial cells activation and/or damage has been reproduced in in vitro and in vivo experimental animal models. Several studies have shown that antibodies reacting with beta2-glycoprotein I, the plasma cofactor for antiphospholipid antibodies, activate endothelial cells. In spite of much in vitro evidence, few studies have addressed the issue as to whether a comparable endothelial perturbation might be detectable in patients with antiphospholipid syndrome. The aim of this study was to evaluate endothelial function in patients with antiphospholipid syndrome. Patients and methods: Flow mediated and glyceryl trinitrate induced dilation of the right brachial artery were studied in 25 healthy controls, 19 patients with first proximal venous thrombosis, 25 patients with primary antiphospholipid syndrome, 25 patients with secondary antiphospholipid syndrome related to systemic lupus crythematosus and 22 patients with systemic lupus erytherrmtosus. Adhesion molecules, tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) antigens and activities, D-dimer, fibrinogen and C-reactive protein (CRP) were measured. Anticardiolipin antibodies, lupus anticoagulant and anti bcta2-glycoprotein I antibodies were detected. Genetic analysis for factor II and factor V Leiden mutations were performed. Results: Flow mediated dilation was significantly lower in patient groups than in controls. Glyceryl trinitrate induced dilation did not differ between the groups. Concentrations of vascular cell adhesion molecule-1 (sVCAM-1), intracellular adhesion molecule (sICAM-1), CRP and fbrinogcn were higher in patients with primary and secondary antiphospholipid syndrome than in healthy controls. (Abstract truncated at 2000 characters)
Deskriptorji		ANTIPHOSPHOLIPID SYNDROME ANTIBODIES, ANTIPHOSPHOLIPID THROMBOSIS ENDOTHELIUM, VASCULAR LUPUS ERYTHEMATOSUS, SYSTEMIC BRACHIAL ARTERY VASODILATION INTERCELLULAR ADHESION MOLECULE-1 VASCULAR CELL ADHESION MOLECULE-1 PLASMINOGEN ACTIVATORS PLASMINOGEN ACTIVATOR INHIBITOR 1 C-REACTIVE PROTEIN FIBRINOGEN