Células endoteliales y micropartículas circulantes en pacientes portadores de anticuerpos antifosfolípidos

Martínez‐Sales, Vicenta; Vila, Virtudes; Micó, Luisa; Contreras, M. Teresa; Escandell, Agusti; Regañón, Edelmiro

doi:10.1016/j.medcli.2010.06.020

Cited by 8 publications

(4 citation statements)

References 9 publications

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“…We found an elevated CEC level in a subgroup of patients with aPL, as previously described in the literature. 18 19 In our study, patients with a medical history of MI or VTE had an increase of CECs, in contrast with results of Cugno et al who did not show a correlation with CECs regarding thrombosis, thrombosis site (i.e., venous or arterial thrombosis), and/or pregnancy losses. 18 The smaller number of patients included in their study may explain this discrepancy by a lack of statistical power.…”

Section: Discussioncontrasting

confidence: 99%

“…15 16 17 While preliminary studies indicate that CECs may be increased in APS, their clinical significance remains to be established. 18 19 Our hypothesis was that increased CECs in patients with aPL is associated with an increased risk for thrombosis. Therefore, our main objective was to quantify CECs in aPL patients and to determine potential associations with other risk factors and thrombosis.…”

Section: Introductionmentioning

confidence: 99%

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Circulating Endothelial Cells are Associated with Thromboembolic Events in Patients with Antiphospholipid Antibodies

et al. 2022

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Background: Endothelium damage has been described in antiphospholipid antibodies (aPL) positive patients. However, it is uncertain whether circulating endothelial cells (CECs) – which are released when endothelial injury occurs – can identify patients at high risk for thrombosis. Methods: Ninety-seven patients with aPL and/or Systemic Lupus Erythematosus (SLE) were included. CECs were determined by an automated CellSearch® system. We also assayed plasma levels of tissue factor-bearing extracellular vesicles (TF+/EVs) and soluble triggering receptor expressed on myeloid cells 1 (sTREM-1) as markers of endothelial dysfunction/damage. Results: Patients mean age was 46.1±13.9 years, 77 were women. Thirty-seven had SLE and 75 patients were suffering from antiphospholipid syndrome. Thirty-seven percent of patients presented a medical history of arterial thrombosis and 46% a history of venous thromboembolism (VTE). Thirteen patients had increased levels of CECs (>20/mL), with a mean CEC level of 48.3±21.3 per mL. In univariate analysis, patients with obesity or medical history of myocardial infarction (MI), VTE or nephropathy had a significant increased CECs level. In multivariate analysis, obesity (OR=6.07 [95% CI; 1.42-25.94]), VTE (OR=7.59 [95% CI; 1.38-41.66]), and MI (OR=5.5 [95% CI;1.1-26.6)] were independently and significantly associated with elevated CECs. We also identified significant correlations between CECs and other markers of endothelial dysfunction: sTREM-1 and TF+/EVs. Conclusions: This study demonstrated that endothelial injury assessed by the levels of CECs was associated with thromboembolic events in patients with aPL and/or autoimmune diseases.

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Section: Discussioncontrasting

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Circulating Endothelial Cells are Associated with Thromboembolic Events in Patients with Antiphospholipid Antibodies

et al. 2022

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“…La lectura del interesante artículo publicado en su revista por Martinez-Sales et al 1 nos sugiere unas reflexiones y comentarios. Los autores estudian la posible relació n entre marcadores de la lesió n endotelial, entre ellos las micropartículas circulantes (MPC) y los anticuerpos antifosfolipídicos (aFL) y/o el síndrome antifosfolipídico (SAF).…”

Section: Sr Editorunclassified

Disfunción endotelial y micropartículas circulantes en pacientes con anticuerpos antifosfolipídicos

Alijotas‐Reig

Palacio-García

2012

Medicina Clínica

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“…Patients with APS exhibit endothelial dysfunction. Mechanistically, vascular alterations in patients with APS, including arterial/venous hyperplasia with occlusion and stenosis in several organs (Amigo and García-Torres, 2000; Martínez-Sales et al, 2011), begins with the binding of aPL to the endothelium. This binding involves the participation of membrane receptors that, in some cases, may require the presence of serum β2GPI (Mineo, 2013; Padjas et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of Endothelial Dysfunction in Antiphospholipid Syndrome: Association With Clinical Manifestations

et al. 2018

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The endothelium is a monolayer of cells that covers the inner surface of blood vessels and its integrity is essential for the maintenance of vascular health. Endothelial dysfunction is a key pathological component of antiphospholipid syndrome (APS). Its systemic complications include thrombotic endocarditis, valvular dysfunction, cerebrovascular occlusions, proliferative nephritis, deep vein thrombosis, and pulmonary embolism. In women, APS is also associated with pregnancy complications (obstetric APS). The conventional treatment regimens for APS are ineffective when the clinical symptoms are severe. Therefore, a better understanding of alterations in the endothelium caused by antiphospholipid antibodies (aPL) may lead to more effective therapies in patients with elevated aPL titers and severe clinical symptoms. Currently, while in vivo analyses of endothelial dysfunction in patients with APS have been reported, most research has been performed using in vitro models with endothelial cells exposed to either patient serum/plasma, monoclonal aPL, or IgGs isolated from patients with APS. These studies have described a reduction in endothelial cell nitric oxide synthesis, the induction of inflammatory and procoagulant phenotypes, an increase in endothelial proliferation, and impairments in vascular remodeling and angiogenesis. Despite these lines of evidence, further research is required to better understand the pathophysiology of endothelial dysfunction in patients with APS. In this review, we have compared the current understanding about the mechanisms of endothelial dysfunction induced by patient-derived aPL under the two main clinical manifestations of APS: thrombosis and gestational complications, either alone or in combination. We also discuss gaps in our current knowledge regarding aPL-induced endothelial dysfunction.

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Células endoteliales y micropartículas circulantes en pacientes portadores de anticuerpos antifosfolípidos

Cited by 8 publications

References 9 publications

Circulating Endothelial Cells are Associated with Thromboembolic Events in Patients with Antiphospholipid Antibodies

Circulating Endothelial Cells are Associated with Thromboembolic Events in Patients with Antiphospholipid Antibodies

Disfunción endotelial y micropartículas circulantes en pacientes con anticuerpos antifosfolipídicos

Mechanisms of Endothelial Dysfunction in Antiphospholipid Syndrome: Association With Clinical Manifestations

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