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This article is part of the supplement: 25th European Workshop for Rheumatology Research

Poster presentation

Endothelial function and activation in women with systemic lupus erythematosus

E Svenungsson, A Cederholm, K Jensen-Urstad, G-Z Fei and J Frostegard

Author Affiliations

Department of Medicine, Rheumatology Unit, Karolinska University Hospital, Solna, Sweden

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Arthritis Research & Therapy 2005, 7(Suppl 1):P148  doi:10.1186/ar1669


The electronic version of this article is the complete one and can be found online at:


Received:11 January 2005
Published:17 February 2005

© 2005 BioMed Central Ltd

Background

Cardiovascular disease (CVD) is common in systemic lupus erythematosus (SLE) patients although it is not clear whether an increased risk of CVD is a general feature of SLE, or whether this applies only to a subgroup of patients.

Objective

To measure early signs of atherosclerosis/vascular dysfunction in women with SLE with or without CVD and in controls, and to investigate whether these correlate to circulating markers of endothelial activation.

Methods

Twenty-six women with SLE and a history of CVD (defined as a history of objectively verified angina pectoris, myocardial infarction, cerebral infarction or intermittent claudication; age 52 ± 8.2 years) were compared with age-matched SLE women without CVD (SLE controls) and population-based age-matched control women (population controls). Flow-mediated dilatation (FMD) of the Brachial artery after reactive hyperemia and after sublingual nitroglycerine administration was performed on women who were not already on nitro-related medication. Levels of thrombomodulin, tumour necrosis factor (TNF) alpha, sTNF receptors, homocysteine and fibrinogen have been associated with endothelial activation/inflammation and were measured in the circulation by use of the ELISA technique.

Results

SLE controls and controls did not differ with respect to FMD after reactive hyperemia or after nitroglycerine administration. Only two SLE cases could be investigated for endothelial function because of nitro-related medication. However, levels of TNF-α, sTNFR1, sTNFR2, and homocysteine discriminated between SLE cases, SLE controls and population controls (P < 0.05 for all), whereas thrombomodulin (P = 0.001) and fibrinogen (P = 0.02) only discriminated between SLE controls and population controls.

Conclusion

Women with SLE who did not have manifest CVD did not differ from age-matched controls with respect to FMD, a measure of endothelial dysfunction. Higher levels of circulating markers of endothelial activation/inflammation were present and discriminated between SLE cases, SLE controls and population controls but these did not correlate to measures of endothelia dysfunction, which may not be a general feature of SLE.