title: Immunological features of primary anti-phospholipid syndrome in connection with endothelial dysfunction.
abstract: OBJECTIVE
  To describe how certain peripheral immune parameters reflect the inflammatory alterations in patients with primary APS.
  
  
  METHODS
  Twenty-eight patients with newly diagnosed primary APS were studied. The control group included 26 patients with stable coronary disease and 38 healthy individuals. Peripheral blood lymphocyte subgroups were quantified, intracellular cytokines were measured by flow cytometry, soluble cytokines and auto-antibodies were assessed using ELISA. Endothelial dysfunction was evaluated by measuring endothelium-dependent (flow-mediated; FMD) vasodilation. Carotid duplex ultrasound was performed to quantify the carotid artery intima-media thickness (IMT). Stiffness parameters, augmentation index (AIx) and pulse wave velocity (PWV) were assessed by TensioClinic technology.
  
  
  RESULTS
  Serum IL-4 and IL-6 levels were significantly higher in APS. CD4+IL10+ and CD8+IL10+ cell percentages in APS were significantly increased compared with controls. Th 0 and T cytotoxic 0 cell percentages were significantly decreased in patients compared with controls. FMD in APS was significantly lower, while IMT was higher than that of controls. FMD showed strong association with stiffness parameters, AIx and PWV. A significant negative linear correlation was detected between PWV and CD8+IL10+ cell percentages and significant positive linear correlation was found between PWV and CD8+IL10- cell percentage.
  
  
  CONCLUSIONS
  In APS, the orchestrated pro-inflammatory cascade can eventually result in endothelial dysfunction, leading to the characteristic vascular abnormalities of the disease.
authors.affiliation: Third Department of Medicine, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary.
authors.forename: P
authors.initials: P
authors.lastname: Soltesz
authors.forename: H
authors.initials: H
authors.lastname: Der
authors.forename: K
authors.initials: K
authors.lastname: Veres
authors.forename: R
authors.initials: R
authors.lastname: Laczik
authors.forename: S
authors.initials: S
authors.lastname: Sipka
authors.forename: G
authors.initials: G
authors.lastname: Szegedi
authors.forename: P
authors.initials: P
authors.lastname: Szodoray
mesh_terms: D016736:Antiphospholipid Syndrome / Q000000981:diagnostic imaging / Q000276:immunology* / Q000503:physiopathology; D015415:Biomarkers / Q000097:blood; D001783:Blood Flow Velocity; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D002339:Carotid Arteries / Q000000981:diagnostic imaging / Q000503:physiopathology; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging; D004548:Elasticity; D004730:Endothelium, Vascular / Q000000981:diagnostic imaging / Q000276:immunology* / Q000503:physiopathology; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007371:Interferon-gamma / Q000097:blood; D016753:Interleukin-10 / Q000097:blood; D015847:Interleukin-4 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008213:Lymphocyte Activation; D018655:Lymphocyte Count; D008297:Male; D018709:Statistics, Nonparametric; D017539:Tunica Intima / Q000000981:diagnostic imaging; D018616:Ultrasonography, Doppler, Duplex; D014652:Vascular Diseases / Q000000981:diagnostic imaging / Q000276:immunology* / Q000503:physiopathology; D014664:Vasodilation
chemical_list: D015415:Biomarkers; D015850:Interleukin-6; D016753:Interleukin-10; D015847:Interleukin-4; D007371:Interferon-gamma