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Rivista di Angiologia

Official Journal of the International Union of Angiology, the International Union of Phlebology and the Central European Vascular Forum
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,899

Periodicità: Bimestrale

ISSN 0392-9590

Online ISSN 1827-1839


International Angiology 2009 Giugno;28(3):192-201

 Original articles

Circulating endothelial cells, endothelial apoptosis and soluble markers of endothelial dysfunction in patients with systemic lupus erythematosus-related vasculitis

Kluz J. 1, Kopec´ W. 2, Jakobsche-Policht U. 1, Adamiec R. 1

1 Department of Angiology, Arterial Hypertension and Diabetology, Wroclaw Medical University, Wroclaw, Poland
2 Department of Nephrology and Transplantation Medicine, Wroclaw Medical University, Wroclaw, Poland

Aim. Evidence is accumulating for endothelial cell dysfunction as one of the main factors initiating vessel wall damage in SLE. Enhanced expression of endothelial adhesion molecules is suggested to play a crucial role in the pathogenesis of vasculitis, while the number of circulating endothelial cells (CECs) is believed to be a reliable marker of endothelial damage. It therefore seems relevant to investigate CECs counts and soluble markers of endothelial dysfunction in SLE patients with inflammatory microangiopathy. The aim of this study was to assess the number of CECs, including apoptotic CECs, as well as to determine serum levels of sVCAM-1, sICAM-1 and sE-selectin in patients with SLE-related vasculitis.
Methods. The study included 51 women with SLE, divided into 2 subgroups: I – patients with severe disease activity according to SLEDAI score, developing vascular complications, such as central nervous system affection and/or vasculitis and/or glomerulonephritis, II – patients with mild or moderate disease activity, without vascular complications. The control group consisted of 16 healthy female volunteers. CECs, including apoptotic CECs, were isolated using anti-CD146-coated immunomagnetic Dynabeads. Serum levels of sVCAM-1, sICAM-1 and sE-selectin levels were determined with ELISA.
Results. In patients with SLE, CEC counts were significantly higher than in healthy controls, and strongly correlated with disease activity assessed by SLEDAI score. The number of apoptotic CECs, as compared with healthy subjects, increased considerably only in subgroup I. Serum sVCAM-1 levels were notably increased in subgroup I in relation to subgroup II and in subgroup II in relation to the control group, while serum sICAM-1 and sE-selectin levels in both subgroups were comparable and significantly higher than those of healthy subjects.
Conclusion. The study showed that the number of CECs increases in SLE and strongly correlates with disease activity, reaching maximum values at the stage of inflammatory microangiopathy-related complications. Severe SLE flares are characterized by enhanced endothelial cell apoptosis. Progressive increase in serum sVCAM-1 levels is connected with disease activity aggravation and development of lupus microangiopathy.

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