Thromb Haemost 1988; 59(01): 080-085
DOI: 10.1055/s-0038-1642570
Review Article
Schattauer GmbH Stuttgart

Thrombosis Associated with Antiphospholipid Antibodies Cannot Be Explained by Effects on Endothelial and Platelet Prostanoid Synthesis

Paula Hasselaar
1   The Department of Haematology, University Hospital Utrecht, The Netherlands
2   The Department of Internal Medicine (Division of Immunopathology), University Hospital Utrecht, The Netherlands
,
Ronald H W M Derksen
2   The Department of Internal Medicine (Division of Immunopathology), University Hospital Utrecht, The Netherlands
,
Laya Blokzijl
1   The Department of Haematology, University Hospital Utrecht, The Netherlands
2   The Department of Internal Medicine (Division of Immunopathology), University Hospital Utrecht, The Netherlands
,
Philip G de Groot
1   The Department of Haematology, University Hospital Utrecht, The Netherlands
› Author Affiliations
Further Information

Publication History

Received 24 August 1987

Accepted after revision 09 October 1987

Publication Date:
18 April 2018 (online)

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Summary

The effect of 23 antiphospholipid antibody positive SLE sera, 4 antiphospholipid antibody negative SLE sera and 17 control sera on endothelial prostacyclin and platelet thromboxane A? production was studied. Endothelial cells and platelets were stimulated with different agonists. Depending on the stimulus used, 4-19% of the SLE sera inhibited the prostacyclin release, whereas 4-28% enhanced prostacyclin production. Our data suggest that the pathophysiological mechanisms underlying decreased prostacyclin production are heterogeneous. Follow-up of two patients showed that prostacyclin inhibitory activity was variable in time. Platelet thromboxane production was normal nr increased, but never decreased in the presence of the SLE sera. An imbalance in thromboxane A2/prostacyclin ratio was present in some patients, but did not correlate with a history of thrombosis. We conclude that, in general, interference of antiphospholipid antibodies with endoihelial or platelet prostanoid synthesis does not explain the occurrence of thromboembolic manifestations in antiphospholipid antibody positive SLE patients.