Does anti-tnf therapy cause any change in platelet activation in ankylosing spondylitis patients?

Örüm, Hüseyin; Pamuk, Gülsüm Emel; Pamuk, Ömer Nurı; Demir, Muzaffer; Turgut, Burhan

doi:10.1007/s11239-011-0663-9

Cited by 10 publications

(7 citation statements)

References 27 publications

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“…Fifteen studies were further excluded for the lack of usable data, and two additional studies were identified though an updated literature search on September 2, 2020 (Supplementary Figure S1). Therefore, 14 published observational studies were finally included (Kisacik et al, 2008;Wang et al, 2008;Yazici et al, 2010;Nalbant et al, 2011;Orum et al, 2012;Boyraz et al, 2014;Bozan et al, 2016;Sezgin et al, 2017;Huang et al, 2018;Tang et al, 2018;Enginar and Kacar, 2019;Al-Osami et al, 2020;Liu et al, 2020;Zhuang et al, 2020). Supplementary Table S2 showed the main characteristics of those observational studies included in the meta-analysis.…”

Section: Significantly Increased Platelet Count In As Patientsmentioning

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: Significantly Increased Platelet Count In As Patientsmentioning

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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“…In our study, E-selectin levels did not differ significantly in both AS and RA patients compared with control group. The cause of subclinical atherosclerosis may be due to platelet parameters, which are another important component in the atherosclerotic process because AS patients have normal endothelial function (19). We also found no significant difference in E-Selectin levels between all patients with rheumatic disease and control group.…”

Section: Discussionmentioning

confidence: 45%

The Relationship Between Disease Activity, Vegf, E-selectin Levels and Arterial Stiffness in Patients with Rheumatic Diseases

Bayğın¹,

Sargın²,

Şentürk³

et al. 2019

Istanbul Med J

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Amaç: Romatoid artrit (RA) ve anklozan spondilitte (AS) endotel hasarı, damar geçirgenliğinde değişim, plak oluşumu kronik enflamasyonda rolleri olan sitokin ve kemokinlerin etkisi ile olmaktadır. Yapılan çalışmalarda enflamasyon düzeyi ile arteryel sertlik ve hücre adezyon molekül miktarında değişim olduğu bildirilmiştir. Bu çalışmada, romatizmal hastalığı olan hastalarda vasküler endotel büyüme faktörü (VEGF), E-selectin, arteriyel sertlik ve hastalık aktivitesi arasındaki ilişkiyi belirlemeyi amaçladık. Yöntemler: Çalışmamıza AS tanılı 13 hasta, RA tanılı 28 hasta ve 30 sağlıklı kontrol dahil edildi. Tüm hasta ve sağlıklı kontrol grubunda arteriyel sertlik, VEGF ve E-selektin, eritrosit sedimentasyon hızı (ESH) ve CRP düzeylerine bakıldı. Romatizmal hastalığı bulunan grupta hastalık aktivite göstergeleri olan Banyo Ankilozan Spondilit Hastalığı Aktivite İndeksi (BASDAİ) ve DAS-28 skorları hesaplandı. Serum VEGF ve E-selektin ölçümü ELISA yöntemi ile, arteriyel sertlik ölçümü ise osilometrik metotla bakıldı. Elde edilen veriler Student t-testi, Mann-Whitney U testi ve Wilcoxon testi ile istatistiksel olarak karşılaştırıldı. Bulgular: Tüm hasta gruplarında tedavi sonrasında 3. ayda DAS-28, BASDAİ skorları, ESH ve CRP düzeylerinde anlamlı bir azalma olduğu gözlenmiştir (p<0,001). Tedavi ile birlikte VEGF ve E-selektin düzeylerinde artış, nabız dalga hızı (NDH) ve artırma indeksi (Alx) parametrelerinde ise azalma olduğu gözlenmiştir. Non-tümör nekroz faktörü tedavisi alan RA hastalarında NDH düzeyi değişmezken, Alx düzeyi tedavinin 3. ayında azalmıştır. Sonuç: RA ve AS hastalarında tedavi ile birlikte inflamasyonun azalması hastalık aktivite skorunda, ESH, CRP değerlerini azaltmaktadır. Arteryel sertlik parametrelerinden NDH ve Alx'i tedavinin 3. ayında azalma ile birlikte anlamlı düzeye ulaşmamıştır. Devam eden tedavi sürecinde arteryel sertliğin ve kardiovasküler riskin anlamlı düzeyde azalacağı düşünülmektedir. Anahtar Kelimeler: Romatoid artrit, ankilozan spondilit, arteriyel sertlik, vasküler endotelyal growth faktör, e-selektin, hastalık aktivitesi Introduction: The endothelial damage, changes in vascular permeability and plaque formation are caused by the effects of cytokines and chemokines that plays role in chronic inflammation in rheumatoid arthritis (RA) and ankylosing spondylitis (AS). It has been reported that arterial stiffness and the level of cell adhesion molecules are affected by inflammation. In this study, we aimed to determine the relationship between vascular endothelial growth factor (VEGF), E-selectin, arterial stiffness and disease activity in patients with rheumatic diseases. Methods: Thirteen patients diagnosed with AS, 28 patients diagnosed with RA and 30 healthy controls were included in the study. Arterial stiffness, VEGF, E-selectin, erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were evaluated in all patients and healthy controls. Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) and Disease Activity Score-28 (DAS-28) were calculated in patients with rhe...

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“…In that study, it was disclosed that anti-TNF-α infusion led to a decrease in serum sE-selectin and sVCAM-1 levels, even if they did not achieve statistical significance [33]. Although some authors also reported a significant reduction in VCAM-1 expression [34] or E-selectin [35] after anti-TNF-α treatment, others did not find any difference in the concentration of these molecules following TNF-α blockade [36,37]. These apparently contradictory results may be due to the period of time elapsed between the assessment of these biomarkers and the time of anti-TNF-α administration.…”

Section: Discussionmentioning

confidence: 99%

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

et al. 2015

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Endothelial dysfunction can be detected by the presence of elevated levels of biomarkers of endothelial cell activation. In this study, we aimed to establish whether correlations of these biomarkers with characteristics of patients with ankylosing spondylitis (AS) exist. We also studied the effect of anti-TNF-α therapy on these biomarkers. Serum sE-selectin, MCP-1 and sVCAM-1 levels were measured by ELISA in 30 non-diabetic AS patients undergoing anti-TNF-α therapy, immediately before and after an infusion of infliximab. Correlations of these biomarkers with clinical features, systemic inflammation, metabolic syndrome and other serum and plasma biomarkers of cardiovascular risk were studied. Potential changes in the concentration of these biomarkers following an infliximab infusion were also assessed. sE-selectin showed a positive correlation with CRP (p = 0.02) and with other endothelial cell activation biomarkers such as sVCAM-1 (p = 0.019) and apelin (p = 0.008). sVCAM-1 negatively correlated with BMI (p = 0.018), diastolic blood pressure (p = 0.008) and serum glucose (p = 0.04). sVCAM-1 also showed a positive correlation with VAS spinal pain (p = 0.014) and apelin (p < 0.001). MCP-1 had a negative correlation with LDL cholesterol (p = 0.026) and ESR (p = 0.017). Patients with hip involvement and synovitis and/or enthesitis in other peripheral joints showed higher levels of MCP-1 (p = 0.004 and 0.02, respectively). A single infliximab infusion led to a significant reduction in sE-selectin (p = 0.0015) and sVCAM-1 (p = 0.04). Endothelial dysfunction correlates with inflammation and metabolic syndrome features in patients with AS. A beneficial effect of the anti-TNF-α blockade on endothelial dysfunction, manifested by a reduction in levels of biomarkers of endothelial cell activation, was observed.

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Does anti-tnf therapy cause any change in platelet activation in ankylosing spondylitis patients?

Cited by 10 publications

References 27 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

The Relationship Between Disease Activity, Vegf, E-selectin Levels and Arterial Stiffness in Patients with Rheumatic Diseases

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

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