ArticleJournal of thrombosis and thrombolysis2012
Does anti-TNF therapy cause any change in platelet activation in ankylosing spondylitis patients? A comparative study.
Article in Journal of thrombosis and thrombolysis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- sCD40 and sCD40L as candidate biomarkers of rheumatic diseases: a systematic review and meta-analysis with meta-regression.Frontiers in immunology · 2025Pooled it
- Adhesion molecules and atherosclerosis in ankylosing spondylitis: implications for cardiovascular risk.Rheumatology international · 2024Review
- Crucial role of lncRNA NONHSAG037054.2 and GABPA, and their related functional networks, in ankylosing spondylitis.Experimental and therapeutic medicine · 2024Article
- Global Proteomic Analyses Reveals Abnormal Immune Regulation in Patients With New Onset Ankylosing Spondylitis.Frontiers in immunology · 2022Article
- Associations of Platelet Count with Inflammation and Response to Anti-TNF-α Therapy in Patients with Ankylosing Spondylitis.Frontiers in pharmacology · 2020Article
- Endothelial dysfunction in patients with ankylosing spondylitis.Reumatologia · 2019Review
- Anti-TNF-α therapy reduces endothelial cell activation in non-diabetic ankylosing spondylitis patients.Rheumatology international · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, it has been reported that ankylosing spondylitis (AS) was characterised by endothelial dysfunction and the development of atherosclerotic complications. In this study, we evaluated platelet and endothelial activation parameters in AS patients. Fiftynine AS patients and 22 healthy controls were included. The clinical features and acute phase parameters were evaluated. In all patients and healthy controls, platelet-monocyte complexes (PMC), platelet-neutrophil complexes, basal and ADP-stimulated P-selectin (CD62P) expression were determined by flow cytometry; soluble E-selectin (sE-selectin) and soluble CD40L (sCD40L) were determined by ELISA. AS patients were divided into two groups as active and inactive by using BASDAI. In 15 AS patients, the evaluated parameters were assessed before and after 12 weeks of anti-TNF therapy. PMC and sCD40L levels in AS patients were significantly higher than in the control group (P values 0.013 and 0.016). The evaluated variables were similar in active and inactive AS groups (P > 0.05). There were no significant changes in platelet and endothelial activation parameters in AS patients after anti-TNF therapy (P > 0.05). Platelet activation which is reflected by high levels of PMC and sCD40L might be responsible for the increased frequency of atherosclerosis in AS. The platelet activation in our AS patients was not associated with disease activity and did not improve after anti-TNF therapy.
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