Anti-TNF-α therapy reduces endothelial cell activation in non-diabetic ankylosing spondylitis patients

Genre, Fernanda; López‐Mejías, Raquel; Miranda‐Filloy, José A.; Ubilla, Begoña; Mijares, Verónica; Carnero-López, Beatriz; Gómez‐Acebo, Inés; Dierssen-Sotos, Trinidad; Remuzgo‐Martínez, Sara; Blanco, Ricardo; Pina, Trinitario; González‐Juanatey, Carlos; Llorca, Javier

doi:10.1007/s00296-015-3314-1

Cited by 27 publications

(9 citation statements)

References 35 publications

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“…The chronic production of C reactive protein (CRP) and inflammatory cytokines such as tumour necrosis factor α and IL-6 may result in a hypercoagulable state 45. Additionally, some studies of patients with AS have demonstrated elevations in E-selectin, MCP-1 and (soluble vascular adhesion molecula-1 (sVCAM-1)46 suggesting possible endothelial dysfunction. Furthermore, there have been some conflicting data with regard to impaired endothelial function as measured by flow-mediated vasodilation, common carotid intima–media thickness and aortic pulse-wave velocity45 in patients with AS.…”

Section: Discussionmentioning

confidence: 99%

Risk of venous thromboembolism in ankylosing spondylitis: a general population-based study

et al. 2019

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BackgroundVenous thromboembolism (VTE), including pulmonary embolism (PE) and deep venous thrombosis (DVT), can be life threatening. An increased frequency of VTE has been found in inflammatory conditions. To date, evidence assessing whether this risk is also greater in patients with ankylosing spondylitis (AS) is scarce.MethodsUsing the provincial British Columbia, Canada healthcare database that encompasses all residents within the province, we conducted matched cohort analyses of incident PE, DVT and overall VTE among incident cases of AS and compared them with individuals randomly selected from the general population without AS. We calculated incidence rates (IRs) of VTE and multivariable analyses after adjusting for traditional risk factors using Cox models.ResultsAmong 7190 incident cases of AS, 35 developed PE and 47 developed DVT. IRs of PE, DVT and overall VTE per 1000 person-years for patients with AS were 0.79, 1.06, 1.56 compared with 0.40, 0.50, 0.77 in the control cohort. Corresponding fully adjusted HRs (95% CI) of PE, DVT and VTE were 1.36 (0.92 to 1.99), 1.62 (1.16 to 2.26) and 1.53 (1.16 to 2.01), respectively. The risks of PE, DVT and VTE were highest in the first year of diagnosis with HR (95% CI) of 2.88 (0.87 to 9.62), 2.20 (0.80 to 6.03) and 2.10 (0.88 to 4.99), respectively.ConclusionsThese findings demonstrate an increased risk of VTE in the general AS population. This risk appears the most prominent in the first year after diagnosis.

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Section: Discussionmentioning

confidence: 99%

Risk of venous thromboembolism in ankylosing spondylitis: a general population-based study

et al. 2019

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“…Increased cardiovascular risk in AS patients and the fact that endothelial dysfunction is reversible after a reduction in atherosclerotic risk factor by life-style modifications and pharmacological treatment [44] provide a strong rationale for early therapeutic intervention. A beneficial effect of infliximab on endothelial dysfunction in non-diabetic AS patients, manifested by a reduction in level of biomarkers of endothelial cell activation such as soluble E-selectin and soluble VCAM-1, was observed by Genre et al [45]. Also, Syngle et al [46] found that infliximab improves both endothelial dysfunction measured by FMD and inflammatory AS activity in previously anti-TNF-naive patients.…”

Section: The Effect Of Drugsmentioning

confidence: 92%

Endothelial dysfunction in patients with ankylosing spondylitis

Łosińska¹,

Korkosz²,

Kwaśny-Krochin³

2019

Reumatologia

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Ankylosing spondylitis (AS) is associated with accelerated atherosclerosis and enhanced cardiovascular morbidity and mortality compared to the general population. The mechanisms and mediators of this phenomenon have not been fully explained, but an expanding body of evidence demonstrates that increased cardiovascular risk in AS is heralded by endothelial dysfunction. We performed a literature review using the PubMed database from the year 2006 up to 2018. In this article we review the epidemiology, current evidence for impaired endothelial function, potential mechanisms and markers controlling this dysfunction, and finally we summarize the data regarding the efficacy of pharmacotherapy in reducing endothelial dysfunction in patients suffering from AS.

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“…111 Interestingly, it has also been shown that just after infliximab infusion, adhesion molecules used as surrogate markers for endothelial activation like sE-selectin, are significantly reduced in AS non-diabetic patients. 112 Treatment with TNFi has also beneficial effects in microvascular function, since endothelium-dependent vasodilation and capillary recruitment was found to be improved in a small cohort of AS patients treated with etanercept for 1 month. 113 Atherosclerotic lesions seem to be significantly improved in SpA patients treated with TNFi.…”

Section: Surrogate Markersmentioning

confidence: 99%

Effect of Biologics on Cardiovascular Inflammation: Mechanistic Insights and Risk Reduction

Fragoulis¹,

Σουλαϊδόπουλος²,

Sfikakis³

et al. 2021

JIR

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It is increasingly recognized that atherosclerosis and consequently cardiovascular disease (CVD) are closely linked with inflammatory processes. The latter is in the center of the pathogenic mechanism underlying autoimmune rheumatic diseases (ARD). It follows then, that optimal control of inflammation in ARDs may lead to a decrease of the accompanied CVD risk. Major trials (eg, CANTOS, CIRT), aimed at examining the possible benefits of immunomodulatory treatments in CVD, demonstrated conflicting results. On the other hand, substantial evidence is accumulating about the possible beneficial effects of biologic disease modifying antirheumatic drugs (bDMARDs) in patients with ARDs, particularly those with rheumatoid arthritis (RA). It seems that bDMARDs (some more than others) alter the lipid profile in RA patients but do not adversely affect, in most cases, the TC/HDL ratio. Favorable effects are noted for arterial stiffness and endothelial function. This is reflected in the lower risk for CVD events, seen in observational studies of RA patients treated with bDMARDs. It should be stressed that more data exist for the TNF-inhibitors than for other bDMARDs, such as tocilizumab, abatacept and rituximab. As regards the spondyloarthropathies (SpA), data are less robust. For TNF-inhibitors, effects appear to be on par with those seen in RA but no conclusions can be drawn for newer biologic drugs used in SpA (eg, IL-17 blockers). Finally, there is accumulating evidence for a beneficial effect of immunosuppressive treatment in cardiac inflammation and function in several ARDs. Introduction of newer therapeutic options in clinical practice seem to have a positive impact on CVD in the setting of ARD. This is probably due to better control of inflammation, but direct improvement in vascular pathology is also a valid hypothesis. Most data are derived from observational studies and, therefore, randomized controlled trials are needed to assess the possible favorable effect of bDMARDs on CVD outcomes.

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Anti-TNF-α therapy reduces endothelial cell activation in non-diabetic ankylosing spondylitis patients

Cited by 27 publications

References 35 publications

Risk of venous thromboembolism in ankylosing spondylitis: a general population-based study

Risk of venous thromboembolism in ankylosing spondylitis: a general population-based study

Endothelial dysfunction in patients with ankylosing spondylitis

Effect of Biologics on Cardiovascular Inflammation: Mechanistic Insights and Risk Reduction

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