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Abstract Number: 20

Complement Deposition On Platelets Is Associated To Venous Thrombosis In Systemic Lupus Erythematosus

Christian Lood1, Helena Tydén1, Birgitta Gullstrand2, Gunnar Sturfelt3, Andreas Jönsen1, Lennart Truedsson2 and Anders A. Bengtsson1, 1Department of Clinical Sciences, Section of Rheumatology, Lund University, Lund, Sweden, 2Department of Laboratory Medicine, Section of Microbiology, Immunology and Glycobiology, Lund University, Lund, Sweden, 3Department of Clinical Sciences Lund, Section of Rheumatology, Lund University, Lund, Sweden

Meeting: ACR/ARHP Annual Meeting 2013

Keywords: Cardiovascular disease, complement, platelets and systemic lupus erythematosus (SLE)

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Session Information

Title: Antiphospholipid Syndrome: Clinical Manifestations and New Biomarkers in Antiphospholipid Syndrome

Session Type: Abstract Submissions (ACR)

Background/Purpose: Anti-phospholipid (aPL) antibodies are associated with development of venous thrombosis and stroke in the autoimmune disease systemic lupus erythematosus (SLE). The underlying mechanism for aPL-mediated thrombosis is not known but may include activation of platelets and the complement system. The aim of this study was to investigate if aPL antibodies could interact with platelets and support complement activation. Furthermore, we investigated if this mechanism was operating in SLE patients and whether complement deposition on platelets was associated to venous thrombosis and specific for SLE.

Methods: Complement deposition was measured by flow cytometry in patients with SLE, rheumatoid arthritis, systemic sclerosis, myocardial infarction and healthy individuals. Associations to cardiovascular disease were analyzed with logistic regression analysis and adjusted for traditional risk factors. Anti-cardiolipin antibodies were used to investigate if aPL antibodies supported platelet activation and complement deposition.

Results: Platelet deposition of C1q and C4d was increased in SLE as compared to healthy individuals (p<0.0001), but high levels were also seen in some patients with rheumatoid arthritis and systemic sclerosis. Complement deposition was clearly associated to venous thrombosis and aPL antibodies in SLE. In vitro, anti-cardiolipin antibodies increased platelet activation and supported C4d deposition on platelets.

Conclusion: Platelet C1q and C4d deposition are identified as markers of venous thrombosis in SLE patients. Several mechanisms are operating in SLE to amplify platelet complement deposition, of which anti-cardiolipin antibodies was identified as one important contributor. Further studies are needed to elucidate the role of platelet complement deposition in development of venous thrombosis.


Disclosure:

C. Lood,
None;

H. Tydén,
None;

B. Gullstrand,
None;

G. Sturfelt,
None;

A. Jönsen,
None;

L. Truedsson,
None;

A. A. Bengtsson,
None.

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