ArticleHaematologica2009
Circulating erythrocyte-derived microparticles are associated with coagulation activation in sickle cell disease.
Article in Haematologica, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03352986 (A Substudy of the CADRE Study), which is not on this map. Cited by 114 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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
A Substudy of the CADRE Study: Determination of Clinical Markers in Patients With Extreme Sickle Cell Disease Phenotype
Who cites it
114 citing papers in PubMed, 1 synthesis or guideline pooled it, 267 citations in OpenAlex.
- Hematological Profile in Sickle Cell Disease: A Systematic Review and Meta-Analysis Comparing Steady-State and Vaso-Occlusive Crisis Phases (2000-2025).BioMed research international · 2026Pooled it
- Association Between Nitric Oxide, Oxidative Stress, Eryptosis, Red Blood Cell Microparticles, and Vascular Function in Sickle Cell Anemia.Frontiers in immunology · 2020Trial
- Trial
- Trial
- Clinical significance of circulating blood and endothelial cell microparticles in sickle-cell disease.Journal of thrombosis and thrombolysis · 2014Trial
- Continuum and discrete modeling of binding-site distribution-mediated reactions on lipid surfaces.Biophysical journal · 2026Article
- Complete Blood Count Profile in Steady State Sickle Cell Disease Patient: A Systematic Review and Meta-Analysis.Health science reports · 2026Article
- Red blood cell-derived transglutaminase 2 influences thrombus formation.Research and practice in thrombosis and haemostasis · 2026Article
- Sickle cell disease: managing thromboembolism.Hematology. American Society of Hematology. Education Program · 2025Review
- Abnormalities of hemostasis in sickle cell patients and predisposition to thrombotic risk: a systematic review and meta-analysis.Thrombosis journal · 2025Review
- Circulating Erythrocyte- and Endothelial-Derived Microvesicles as Biomarkers of Hemolysis and Clinical Severity in Sickle Cell Disease.Journal of cellular and molecular medicine · 2025Article
- An update on recent studies of extracellular vesicles and their role in hypercoagulability in thalassemia (Review).Biomedical reports · 2024Review
- Missing the mark(ers): circulating endothelial cells and endothelial-derived extracellular vesicles are elevated in sickle cell disease plasma.Frontiers in immunology · 2024Article
- Plasma levels of BCMA-positive extracellular vesicles correlate to response and side effects in myeloma patients treated with belantamab-mafodotin.Oncotarget · 2023Article
- Extracellular vesicles in venous thromboembolism and pulmonary hypertension.Journal of nanobiotechnology · 2023Review
- VWF-ADAMTS13 axis dysfunction in children with sickle cell disease treated with hydroxycarbamide vs blood transfusion.Blood advances · 2023Article
- Predisposing Factors and Incidence of Venous Thromboembolism among Hospitalized Patients with Sickle Cell Disease.Journal of clinical medicine · 2023Article
- Association of Circulating Procoagulant Microvesicles with Painful Vaso-Occlusive Crisis in Sickle Cell Disease.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2023Article
- Sickle red blood cell-derived extracellular vesicles activate endothelial cells and enhance sickle red cell adhesion mediated by von Willebrand factor.British journal of haematology · 2023Article
- Factor XII contributes to thrombotic complications and vaso-occlusion in sickle cell disease.Blood · 2023Article
54 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSickle cell disease is characterized by a hypercoagulable state as a result of multiple factors, including chronic hemolysis and circulating cell-derived microparticles. There is still no consensus on the cellular origin of such microparticles and the exact mechanism by which they may enhance coagulation activation in sickle cell disease. DESIGN AND
methodsIn the present study, we analyzed the origin of circulating microparticles and their procoagulant phenotype during painful crises and steady state in 25 consecutive patients with sickle cell disease.
resultsThe majority of microparticles originated from platelets (GPIIIa,CD61) and erythrocytes (glycophorin A,CD235), and their numbers did not differ significantly between crisis and steady state. Erythrocyte-derived microparticles strongly correlated with plasma levels of markers of hemolysis, i.e. hemoglobin (r=-0.58, p<0.001) and lactate dehydrogenase (r=0.59, p<0.001), von Willebrand factor as a marker of platelet/endothelial activation (r=0.44, p<0.001), and D-dimer and prothrombin fragment F1+2 (r=0.52, p<0.001 and r=0.59, p<0.001, respectively) as markers of fibrinolysis and coagulation activation. Thrombin generation depended on the total number of microparticles (r=0.63, p<0.001). Anti-human factor XI inhibited thrombin generation by about 50% (p<0.001), whereas anti-human factor VII was ineffective (p>0.05). The extent of factor XI inhibition was associated with erythrocyte-derived microparticles (r=0.50, p=0.023).
conclusionsWe conclude that the procoagulant state in sickle cell disease is partially explained by the factor XI-dependent procoagulant properties of circulating erythrocyte-derived microparticles.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.