Thrombosis risk in systemic lupus erythematosus: the role of thrombophilic risk factors

Sallai, Krisztina; Nagy, Eszter; Bodó, Imre; Mohl, A.; Palla, Gergely

doi:10.1080/03009740601089283

Cited by 32 publications

(29 citation statements)

References 43 publications

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“…These antibodies could also induce endothelial damage in a similar way. In fact, it was demonstrated that some specific autoantibodies against phospholipids can activate endothelial cells, inducing membrane expression of ICAM-1, VCAM-1, and E-selectin and also increases the expression of tissue factor in endothelial cells and monocytes from SLE patients [45]. …”

Section: Endothelial Alterations In Sle and Ra: Potential Contribumentioning

confidence: 99%

Endothelial Alterations in Systemic Lupus Erythematosus and Rheumatoid Arthritis: Potential Effect of Monocyte Interaction

Atehortúa

Rojas

Vásquez

et al. 2017

Mediators of Inflammation

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Patients with systemic autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) are prone to develop atherosclerosis and cardiovascular diseases five times more often than the general population; this increase in frequency could be partially explained by an increase in the macrovasculature endothelial damage. In these autoimmune diseases, a microvascular endothelial injury has also been reported in different organs and tissues, especially in sites where ultrafiltration processes occur. Different components that are characteristic to the immunopathology of RA and SLE could be involved in the endothelial cell activation, permeability increase, functional alteration, and vascular injury. Circulating immune complexes (IC) detected in SLE and RA have been proposed to participate in the endothelial injury. In the vascular environment, IC can generate different responses that could be mediated by monocytes, because these cells have patrolling and monitoring functions on the endothelium. However, with certain stimuli such as TLR ligands, the monocytes are retained in the lumen, releasing proinflammatory mediators that participate in the endothelial damage. This paper aims to review some aspects about the endothelial activation and dysfunction in the context of SLE and RA, as well as the potential role that monocytes apparently play in this process.

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Section: Endothelial Alterations In Sle and Ra: Potential Contribumentioning

confidence: 99%

Endothelial Alterations in Systemic Lupus Erythematosus and Rheumatoid Arthritis: Potential Effect of Monocyte Interaction

Atehortúa

Rojas

Vásquez

et al. 2017

Mediators of Inflammation

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“…There are three main aPL tests used in clinical practice; anti-cardiolipin (aCL) antibodies, anti-beta 2 glycoprotein I (aB2GPI) antibodies and lupus anticoagulans (LA). Positivity in one or more of those assays is associated with development of venous thrombosis and stroke [6], [7], [8], [9]. The underlying mechanism of aPL antibody-mediated thrombosis is not fully understood.…”

Section: Introductionmentioning

confidence: 99%

Platelet Activation and Anti-Phospholipid Antibodies Collaborate in the Activation of the Complement System on Platelets in Systemic Lupus Erythematosus

et al. 2014

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Anti-phospholipid (aPL) antibodies are important contributors to development of thrombosis in patients with the autoimmune rheumatic disease systemic lupus erythematosus (SLE). The underlying mechanism of aPL antibody-mediated thrombosis is not fully understood but existing data suggest that platelets and the complement system are key components. Complement activation on platelets is seen in SLE patients, especially in patients with aPL antibodies, and has been related to venous thrombosis and stroke. The aim of this study was to investigate if aPL antibodies could support classical pathway activation on platelets in vitro as well as in SLE patients. Furthermore, we investigated if complement deposition on platelets was associated with vascular events, either arterial or venous, when the data had been adjusted for traditional cardiovascular risk factors. Finally, we analyzed if platelet complement deposition, both C1q and C4d, was specific for SLE. We found that aPL antibodies supported C4d deposition on platelets in vitro as well as in SLE patients (p = 0.001 and p<0.05, respectively). Complement deposition on platelets was increased in SLE patients when compared with healthy individuals (p<0.0001). However, high levels of C4d deposition and a pronounced C1q deposition were also seen in patients with rheumatoid arthritis and systemic sclerosis. In SLE, C4d deposition on platelets was associated with platelet activation, complement consumption, disease activity and venous (OR = 5.3, p = 0.02), but not arterial, thrombosis, observations which were independent of traditional cardiovascular risk factors. In conclusion, several mechanisms operate in SLE to amplify platelet complement deposition, of which aPL antibodies and platelet activation were identified as important contributors in this investigation. Complement deposition on platelets was identified as a marker of venous, but not arterial thrombosis, in SLE patients independently of traditional risk factors and aPL antibodies. Further studies are needed to elucidate the role of complement deposition on platelets in development of venous thrombosis.

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“…A combination of traditional and non-traditional risk factors may account for this increased risk, such as dyslipidaemia and hypertension or kidney involvement; systemic inflammation including C-reactive protein (CRP), tumour necrosis factor alpha (TNF-a), and platelet activating factor (PAF)-acetylhydrolase; and raised lipid peroxidation and anti-phospholipid antibodies (aPL) (2)(3)(4)(5). Increased prevalence of atherosclerotic plaques in SLE and also in association with CVD in SLE has been reported by several groups (3,(6)(7)(8).…”

mentioning

confidence: 99%

Dyslipidaemia and lipoprotein pattern in systemic lupus erythematosus (SLE) and SLE‐related cardiovascular disease

Xiang

Sawada

Svenungsson

et al. 2009

Scandinavian Journal of Rheumatology

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Thrombosis risk in systemic lupus erythematosus: the role of thrombophilic risk factors

Abstract: In SLE patients, the presence of aPL is a more significant risk factor for the development of thrombosis than the known inherited deficiencies. Based on these data, routine screening for additional hereditary risk factors seems to be unwarranted.

Cited by 32 publications

References 43 publications

Endothelial Alterations in Systemic Lupus Erythematosus and Rheumatoid Arthritis: Potential Effect of Monocyte Interaction

Endothelial Alterations in Systemic Lupus Erythematosus and Rheumatoid Arthritis: Potential Effect of Monocyte Interaction

Platelet Activation and Anti-Phospholipid Antibodies Collaborate in the Activation of the Complement System on Platelets in Systemic Lupus Erythematosus

Dyslipidaemia and lipoprotein pattern in systemic lupus erythematosus (SLE) and SLE‐related cardiovascular disease

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