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Updated: May 25, 2026

Routine Screening Method for Microparticles in Platelet Transfusions
Published on: January 31, 2018
Evaluation of circulating endothelial and platelet microparticles in men with ankylosing spondylitis
Ismail Sari1, Giray Bozkaya, Halil Kirbiyik
1Department of Internal Medicine, Division of Rheumatology, Dokuz Eylul Universitesi School of Medicine, Izmir, Turkey. ismailsari35@gmail.com
Objective:
To evaluate the profiles of endothelial microparticles (EMP) and platelet microparticles (PMP) in men with ankylosing spondylitis (AS) and healthy subjects. We also aimed to determine whether microparticles (MP) correlate with disease activity, function, and spinal mobility indices.
Methods:
There were 82 men with AS and 53 healthy controls. Subjects with a history of chronic diseases including coronary artery disease, hypertension, diabetes mellitus, and dyslipidemia were excluded. MP were stained with monoclonal antibodies against platelets and endothelial cells and quantified using flow cytometry. MP that were positive for both CD42a+/CD31+ and total CD42a+ were identified as PMP; and MP consisting of CD42a-/CD31+ and total CD144+ were considered EMP.
Results:
EMP and PMP were similar between the patient and control groups (p > 0.05). Comparison of patients with AS in the active disease state (BASDAI ≥ 4) and in the inactive state showed that EMP and PMP were not different between the groups (p > 0.05). Correlation analysis revealed no correlation with Bath Ankylosing Spondylitis Disease Activity Index, Bath Ankylosing Spondylitis Functional Index, or Bath Ankylosing Spondylitis Metrology Index. C-reactive protein was significantly correlated with PMP and CD42a-/CD31+ EMP (p < 0.05). Comparison of patients with AS treated with anti-tumor necrosis factor (anti-TNF) drugs, subjects treated conventionally, and healthy controls revealed that PMP and CD42a-/CD31+ EMP were significantly downregulated in patients receiving biological agents.
Conclusion:
Circulating EMP and PMP, known to be indicators and mediators of vascular injury, were not significantly altered in men with AS who did not have classical cardiovascular risk factors. Significantly downregulated MP in patients receiving biological agents suggested that anti-TNF treatment may have a beneficial effect on vascular function in AS.
Insights
Endothelial and platelet microparticles were similar in men with ankylosing spondylitis (AS) and controls, but downregulated with anti-TNF therapy. This suggests anti-TNF treatment may benefit vascular function in AS patients.
Area of Science:
- Rheumatology and Immunology
- Vascular Biology
- Biomarker Discovery
Background:
- Ankylosing spondylitis (AS) is a chronic inflammatory disease affecting the spine.
- Vascular dysfunction is a concern in AS, potentially mediated by microparticles.
- Endothelial microparticles (EMP) and platelet microparticles (PMP) are cell-derived vesicles linked to vascular injury.
Purpose of the Study:
- To compare EMP and PMP levels in men with AS versus healthy controls.
- To investigate the correlation of EMP and PMP with AS disease activity and spinal mobility.
- To assess the impact of anti-tumor necrosis factor (anti-TNF) therapy on EMP and PMP levels in AS.
Main Methods:
- Flow cytometry was used to quantify EMP and PMP in 82 men with AS and 53 healthy controls.
- Exclusion criteria included subjects with pre-existing cardiovascular risk factors.
- Specific antibody markers (CD42a, CD31, CD144) identified EMP and PMP.
Main Results:
- No significant differences in EMP or PMP were found between AS patients and controls.
- EMP and PMP levels did not correlate with disease activity indices (BASDAI, BASFI, BASMI).
- PMP and a subset of EMP (CD42a-/CD31+) were significantly lower in AS patients treated with anti-TNF agents.
Conclusions:
- Circulating EMP and PMP are not significantly altered in AS patients without traditional cardiovascular risk factors.
- Downregulation of EMP and PMP in patients on anti-TNF therapy suggests a potential vascular benefit.
- Anti-TNF treatment may positively influence vascular health in ankylosing spondylitis.

