Measuring Choroid Thickness as a Marker of Systemic Inflammation in Patients With Ankylosing Spondylitis

Steiner, Martina; Esteban-Ortega, M. D. M.; Thuissard-Vasallo, I.J.; García-Lozano, I; Moriche-Carretero, Manuel; García-González, Alejandro Javier; Pérez-Blázquez, Eugenio; Sambricio, Javier; García‐Aparicio, Ángel; Casco-Silva, Bruno Francisco; Sanz, Jesús; Valdés-Sanz, Nuria; Fernández-Espartero, Cruz; Diaz-Valle, Teresa; Gurrea-Almela, María; Fernández-Melón, Julia; Gómez-Resa, María; Pato-Cour, Esperanza; Díaz-Valle, D.; Méndez-Fernández, R.; Marco, Teresa Navío; Almodóvar, Raquel; García-Sáenz, M.C.; Del-Prado-Sánchez, Cristina

doi:10.1097/rhu.0000000000001348

Cited by 3 publications

(4 citation statements)

References 22 publications

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“…Platelet parameters have been suggested as important markers of inflammation ( Bilen et al, 2015 ; Kalelioglu et al, 2015 ; Akboga et al, 2016 ; Koupenova et al, 2018 ). Unlike other rheumatic disease such as SLE and Sjögren’s syndrome (SjS), AS is a rheumatic disease characterized by serious inflammatory responses ( Vanaki et al, 2018 ; Vinker Shuster et al, 2018 ; Steiner et al, 2020 ). It has been clear that inflammation has a crucial role in the development of AS ( Machado et al, 2016 ; Tseng et al, 2016 ; Ranganathan et al, 2017 ).…”

Section: Discussionmentioning

confidence: 99%

Associations of Platelet Count with Inflammation and Response to Anti-TNF-α Therapy in Patients with Ankylosing Spondylitis

et al. 2020

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Background: Increased platelet count has been reported in ankylosing spondylitis (AS) patients, but its clinical significance is still largely elusive. The objective of this study was to evaluate the clinical role of platelet count in AS patients, especially its impact on treatment outcomes. Methods: A case-control study containing 35 AS patients receiving anti-tumor necrosis factor-α (anti-TNF-α) therapy and 45 healthy controls was performed, and AS patients were followed at least 6 months after anti-TNF-α therapy. A systematic review and metaanalysis of studies containing relevant data on outcomes of interest was also performed. Results: AS patients had significantly higher platelet count than controls (p 0.0001), and the significantly increased platelet count in AS patients was confirmed in a metaanalysis of 14 studies involving 1,223 AS patients and 913 controls (mean difference 39.61, 95% CI 27.89-51.34, p < 0.001). Besides, platelet count was significantly correlated with ESR (p < 0.001) and was moderately correlated with ASDAS-CRP score (p 0.002). Moreover, anti-TNF-α therapy could reduce platelet count in AS patients at the first month and the effect was maintained through the treatment duration. In the prospective follow-up study of those 35 AS patients, those responders to anti-TNF-α therapy had significantly lower platelet count than nonresponders (p 0.015). Logistic regression analysis suggested that lower platelet count was associated with higher possibility of achieving good response to anti-TNF-α therapy in AS patients (odds ratio 2.26; 95% CI 1.06-4.82; p 0.035). Conclusion: This study suggested that platelet count was associated with inflammation severity and treatment outcomes in AS patients, and elevated platelet count was a promising biomarker of poorer response to anti-TNF-α therapy. The findings above need to be validated in more future studies.

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Section: Discussionmentioning

confidence: 99%

Associations of Platelet Count with Inflammation and Response to Anti-TNF-α Therapy in Patients with Ankylosing Spondylitis

et al. 2020

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“…Ankylosing spondylitis (AS) is a chronic autoimmune inflammatory disease that primarily invades the spine and involves the cuboid iliac joint (1). The disability rate of patients with AS is high and AS has a serious impact on quality of life (2,3). Studies have shown that AS is associated with genetics, infection, immunity, inflammatory cell infiltration, cytokine imbalance and other factors (4,5).…”

Section: Introductionmentioning

confidence: 99%

Acrylamide induces human chondrocyte cell death by initiating autophagy‑dependent ferroptosis

Wang

Tang

et al. 2023

Exp Ther Med

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Acrylamide (ACR) is formed during heat treatment of foodstuffs and ACR may serve as a probable malignant neoplastic disease agent in all organs and tissues of the human body. However, it is unknown if ACR is associated with ankylosing spondylitis (AS) pathogenesis. Cell viability and proliferation were determined using CCK-8 assay and EdU staining. Flow cytometry was used to determine cell death and cell cycle arrest. Intracellular lipid reactive oxygen species, Fe 2+ and mitochondrial membrane potential (MMP) were analyzed using a C11-BODIPY581/591 fluorescent probe, FerroOrange staining and a JC-1 MMP Assay kit, respectively. The present study showed that ACR decreased chondrocyte cell viability in a dose-dependent manner and that ACR significantly promoted chondrocyte senescence. ACR also elevated the expression of cell cycle arrest-associated proteins, including p53, cyclin-dependent kinase inhibitor 1 and cyclin-dependent kinase inhibitor protein, in human chondrocytes. Similarly, DNA damage was also enhanced following ACR treatment in chondrocytes. In addition, the ferroptosis-specific inhibitor ferrostatin-1 (Fer-1) and the autophagy inhibitor 3-methyladenine abolished ACR-induced cell death in chondrocytes. ACR was shown to activate autophagic flux and induce mitochondrial dysfunction by increasing the MMP. Western blot analysis of ferroptosis-related proteins demonstrated that ACR decreased the expression of glutathione peroxidase 4, solute carrier family 7 member 11, transferrin receptor protein 1 and ferritin heavy chain 1 in chondrocytes whereas Fer-1 abolished these effects. ACR treatment significantly elevated the phosphorylation levels of AMP-activated protein kinase (AMPK) and serine/threonine-protein kinase ULK1 in human chondrocytes. Notably, the effect of ACR was diminished by knockdown of AMPK, as evidenced by reduced lipid reactive oxygen species accumulation and Fe 2+ levels. Hence, ACR inhibited cell proliferation and contributed to cell death by inducing autophagy-dependent ferroptosis while promoting autophagy by activating AMPK-ULK1-mTOR signaling in human chondrocytes. It was hypothesized that the presence of ACR in foodstuffs may increase the risk of AS and that decreasing ACR in food products is of importance.

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“…9 Patients with AS without eye inflammation and high disease activity have a significantly thicker choroid than healthy subjects. 10 In this study, we hypothesized that CT decreases after biological treatment, therefore acting as a marker of systemic inflammation in patients with AS. This study aimed to compare CT in biological treatment-naive disease-active patients before and after 6 months of therapy.…”

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confidence: 99%

“…Patients with AS without eye inflammation and high disease activity have a significantly thicker choroid than healthy subjects 10 …”

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confidence: 99%

Choroidal Thickness Is a Biomarker Associated With Response to Treatment in Ankylosing Spondylitis

et al. 2020

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and on behalf of the ChOroidal Thickness in ESpondylitis (COnTEST) Study Group Objective: Choroidal thickness (CT) has been evaluated as a marker of systemic inflammation in ankylosing spondylitis (AS). This study evaluates the CT of AS patients before and after 6 months of biological treatment.Methods: This longitudinal multicenter study evaluated CT in 44 AS patients. The correlations between CT and C-reactive protein (CRP) with disease activity indices were calculated. The concordance between CT and CRP was determined. We assessed factors associated with response to treatment. Clinically important improvement was defined as a decrease in Ankylosing Spondylitis Disease Activity Score of 1.1 points or greater.Results: Forty-four eyes in patients aged 18 to 65 years were included. Mean CT values were significantly higher at baseline than after 6 months of treatment (baseline: 355.28 ± 80.46 μm; 6 months: 341.26 ± 81.06 μm; p < 0.001). There was a 95% concordance between CT and CRP at baseline and 6 months. Clinically important improvement was associated with lower baseline CT and age as independent factors (odds ratios, 0.97 [95% confidence interval, 0.91-0.93; p = 0.009] and 0.81 [95% confidence interval, 0.7-0.95; p = 0.005]), with baseline CT of less than 374 μm (sensitivity 78%, specificity 78%, area under the curve 0.70, likelihood ratio 3.6).Conclusions: Choroidal thickness decreased significantly after 6 months of biological treatment in all treatment groups. Choroidal thickness and CRP had a 95% concordance. A high CTwas associated with a risk of biological treatment failure. Choroidal thickness can be considered a useful biomarker of inflammation and a factor associated with response to treatment in AS.

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Measuring Choroid Thickness as a Marker of Systemic Inflammation in Patients With Ankylosing Spondylitis

Cited by 3 publications

References 22 publications

Associations of Platelet Count with Inflammation and Response to Anti-TNF-α Therapy in Patients with Ankylosing Spondylitis

Associations of Platelet Count with Inflammation and Response to Anti-TNF-α Therapy in Patients with Ankylosing Spondylitis

Acrylamide induces human chondrocyte cell death by initiating autophagy‑dependent ferroptosis

Choroidal Thickness Is a Biomarker Associated With Response to Treatment in Ankylosing Spondylitis

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