ArticleArthritis research & therapy2013
Contact activation products are new potential biomarkers to evaluate the risk of thrombotic events in systemic lupus erythematosus.
Article in Arthritis research & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 21 citations in OpenAlex.
- Molecular determinants of thromboinflammatory activation in inflammatory bowel disease.Journal of molecular medicine (Berlin, Germany) · 2026Review
- Prompt Thrombo-Inflammatory Response to Ischemia-Reperfusion Injury and Kidney Transplant Outcomes.Kidney international reports · 2023Article
- Distinction of early complement classical and lectin pathway activationFrontiers in immunology · 2022Article
- C1 inhibitor-mediated myocardial protection from chronic intermittent hypoxia-induced injury.Experimental and therapeutic medicine · 2016Article
- Complement inhibition in biomaterial- and biosurface-induced thromboinflammation.Seminars in immunology · 2016Review
- Evasion and interactions of the humoral innate immune response in pathogen invasion, autoimmune disease, and cancer.Clinical immunology (Orlando, Fla.) · 2015Review
- Imbalance between endothelial damage and repair: a gateway to cardiovascular disease in systemic lupus erythematosus.BioMed research international · 2014Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionPatients with systemic lupus erythematosus (SLE) have persistent platelet activation and an increased risk of thrombotic events, which cannot be accounted for by traditional cardiovascular risk factors. Factor (F)XII has a potentially important role in thrombus formation and is triggered by activated platelets. We therefore asked whether the contact system is involved in inflammation and vascular disease (VD) in SLE.
methodsFibrin clots were incubated with purified FXII or whole blood, and the activation and regulation of FXII were studied. Plasma from SLE patients with (n = 31) or without (n = 38) previous VD and from matched healthy controls (n = 68) were analyzed for the presence of complexes formed between contact system enzymes and antithrombin (AT) or C1 inhibitor (C1INH) and evaluated with regard to clinical data and laboratory parameters.
resultsFibrin clots elicited FXII activation and acted as co-factors for AT. In clotting plasma, the levels of FXIIa-AT increased, and FXIIa-C1INH decreased. A similar reciprocal relationship existed in SLE patients. FXIIa-AT was elevated in the SLE patients with a history of VD, while the corresponding levels of factor FXIIa-C1INH were significantly decreased. FXIIa-AT correlated strongly with platelet parameters. The odds ratio for VD among the SLE patients was 8.9 if they had low levels of FXIIa-C1INH, 6.1 for those with high levels of FXIIa-AT, and increased to 23.4 for those with both decreased levels of FXIIa-C1INH and increased levels of FXIIa-AT.
conclusionsActivation of FXII is elicited by fibrin during thrombotic reactions in vitro and in vivo, and fibrin acts as a heparin-like co-factor and regulates AT. Patients with SLE had altered levels of FXIIa-serpin complexes, supporting that the contact system is involved in this disease. FXIIa-serpin complexes are strongly associated with previous VD in SLE patients, suggesting that these complexes are potential biomarkers for monitoring and assessing the risk of thrombotic events in SLE.
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