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Thromb Haemost 1989; 61(01): 097-100
DOI: 10.1055/s-0038-1646534
Original Article
Schattauer GmbH Stuttgart

Endothelial Prostacyclin Release in Systemic Lupus Erythematosus

Stephen B Coade
1   The Section of Vascular Biology, MRC Clinical Research Centre, Harrow, Middx, UK
,
Els van Haaren
1   The Section of Vascular Biology, MRC Clinical Research Centre, Harrow, Middx, UK
,
S Loizou
3   The Department of Medicine, Royal Postgraduate Medical School, Hammersmith, London, UK
,
Mark J Walport
3   The Department of Medicine, Royal Postgraduate Medical School, Hammersmith, London, UK
,
A Michael Denman
2   The Division of Rheumatology, MRC Clinical Research Centre, Harrow, Middx, UK
,
Jeremy D Pearson
1   The Section of Vascular Biology, MRC Clinical Research Centre, Harrow, Middx, UK
› Author Affiliations
Further Information

Publication History

Received 03 May 1988

Accepted after revision 21 September 1988

Publication Date:
24 July 2018 (online)

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Summary

The ability of sera from patients with SLE to stimulate endothelial cell prostacyclin production was studied using a standardized assay system for testing the effects of serum on cultured human endothelial cell monolayers. The effects of 20 normal and 32 SLE sera on endothelial prostacyclin production were measured. No differences between the rates of prostacyclin production were seen between the two groups, either basally or when prostacyclin release was stimulated with thrombin or bradykinin. In the SLE samples there was no correlation between anticardiolipin IgG or IgM titres and their ability to stimulate basal or agonist-induced prostacyclin release. These results suggest that the elevated risk of thrombosis in SLE patients is not associated with inhibition of endothelial cell prostacyclin synthesis.

Keywords

SLE - Prostacyclin - Endothelium - Lupus anticoagulant - Anticardiolipin antibodies
 

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