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Platelet aggregation, secretion, and coagulation changes in children with asthma
Gonul Buyukyilmaz1, Ozge U Soyer, Betul Buyuktiryaki
1aDepartment of Pediatrics, Ankara Education and Research Hospital, The Ministry of Health of Turkey bDepartment of Pediatric Allergy, Hacettepe University, School of Medicine cDepartment of Pediatric Hematology, The Ministry of Health of Turkey, Ankara Education and Research Hospital, Ankara, Turkey *Gonul Buyukyilmaz and Ozge U. Soyer contributed equally to this article.
Insights
Platelets play a role in asthma. Children with asthma attacks showed reduced platelet secretion and higher levels of von Willebrand factor (vWF) and factor VIII (FVIII), suggesting coagulation mechanisms are key in asthma.
Area of Science:
- Pediatric Allergy and Immunology
- Hematology
- Respiratory Medicine
Background:
- Asthma involves chronic inflammation mediated by various immune cells.
- Platelets, primarily known for hemostasis, are increasingly recognized for their role in asthma pathogenesis, particularly during antigen provocation and exacerbations.
Purpose of the Study:
- To investigate platelet function and hemostatic markers in children with asthma.
- To compare these parameters during symptom-free periods versus asthma attacks.
Main Methods:
- Evaluated platelet aggregation and secretion (ATP release) using a lumiaggregometer with various agonists (collagen, epinephrine, ADP, thrombin, ristocetin, arachidonic acid).
- Assessed plasma levels of D-dimer, factor VIII (FVIII), and von Willebrand factor (vWF).
- Included children with asthma attacks, mild intermittent asthma, mild persistent asthma, and healthy controls.
Main Results:
- No significant differences in agonist-induced platelet aggregation were observed between groups.
- Platelet ATP release stimulated by ADP and epinephrine was significantly lower in children experiencing asthma attacks compared to other groups and controls.
- Plasma vWF levels were elevated in children with asthma attacks, and FVIII levels increased in those with severe attacks.
Conclusions:
- Platelet secretion profiles differ in children with asthma attacks.
- Elevated vWF and FVIII levels in asthma exacerbations suggest a role for coagulation pathways.
- These findings highlight the potential critical involvement of coagulation mechanisms in asthma pathogenesis.
Abstract:
The chronic inflammation in asthma evolves by cells including eosinophils, mast cells and lymphocytes. Despite their principal function in hemostasis, platelets contribute to pathogenesis of asthma that activation of platelets occurs following antigen provocation and during asthma attack. Our aim was to evaluate the platelet functions and other hemostatic features of children with asthma, both during symptom-free period and asthma attack. We enrolled patients with asthma attack (n = 33), mild intermittent asthma (n = 18), mild persistent asthma (n = 15) and healthy children (n = 20). Demographic characteristics and disease-related features were noted. Platelet aggregation and secretion tests (expressed as ATP release) were performed by lumiaggregometer method by stimulation with collagen, epinephrine, ADP, thrombin, ristocetin and arachidonic acid. Plasma levels of D-dimer, factor VIII (FVIII) and von Willebrand factor (vWF) were assessed. There were no differences in platelet aggregation induced by agonists between study groups. ATP release from platelets of patients with asthma exacerbation induced by ADP was lower compared with mild intermittent asthma (P < 0.001). Epinephrine-stimulated ATP secretion was also lower in patients with asthma attack than mild intermittent (P = 0.039) and mild persistent asthma (P = 0.011) and controls (P = 0.018). vWF measurements were higher in children with asthma attack than other study groups (P = 0.001). However, FVIII was increased in patients with severe asthma attack. Asthma is a disease in which many immune cells play a role, one of which is the platelet. Distinctions in platelet secretion profiles and plasma levels of vWF and FVIII provide evidence that coagulation mechanisms might be critical for asthma pathogenesis.