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Analyzing Platelet Subpopulations by Multi-color Flow Cytometry
Published on: June 10, 2025
Platelet and other hemostatic characteristics in patients with chronic urticaria
Nilgun Isiksacan1, Murat Koser2, Ferhan Cemsitoglu3
1Central Laboratory, Dr Sadi Konuk Training and Research Hospital, Bakirkoy, Istanbul, Turkey.
Insights
Platelet aggregation was reduced in chronic urticaria (CU) patients, with elevated D-dimer levels indicating activated coagulation and fibrinolysis. These findings suggest platelets play a role in CU development.
Area of Science:
- Immunology
- Hematology
- Dermatology
Background:
- Coagulation and fibrinolysis are implicated in chronic urticaria (CU).
- The specific role of platelets in CU pathogenesis requires further elucidation.
Purpose of the Study:
- To assess platelet aggregation in patients with CU.
- To evaluate coagulation and fibrinolysis parameters in CU patients.
Main Methods:
- Platelet aggregation was measured using an impedance aggregometer with various agonists (ADP, arachidonic acid, TRAP, ristocetin).
- Coagulation and fibrinolysis markers, including D-dimer and mean platelet volume, were analyzed.
- 34 CU patients and 36 healthy controls were included.
Main Results:
- Patients with CU showed significantly decreased platelet aggregation in response to ristocetin and thrombin receptor-activating peptide (TRAP).
- Elevated D-dimer levels and decreased mean platelet volume were observed in CU patients.
- No significant alterations were found in other coagulation assays.
Conclusions:
- Activated coagulation and fibrinolysis are indicated in CU patients by elevated D-dimer levels.
- Altered platelet function, specifically reduced aggregation, may contribute to the pathogenesis of chronic urticaria.
- Further evaluation of platelet function could clarify their role in CU.
Abstract:
Several publications have pointed out the importance of coagulation and fibrinolysis in the occurrence of chronic urticaria (CU), but only a few indicated the direct role of platelets. We assessed platelet aggregation and evaluated parameters of coagulation and fibrinolysis in patients with CU. Patients (n = 34) diagnosed as having CU and 36 healthy controls were enrolled. Platelet aggregation was assayed using an impedance aggregometer and adenosine diphosphate, arachidonic acid, thrombin receptor-activating peptide (TRAP), and ristocetin as agonists. In patients with CU, significantly decreased platelet aggregation to some agonists (ristocetin and TRAP) was observed. The D-dimer levels were elevated, mean platelet volume was decreased, but no alteration was observed in other coagulation assays. Elevated D-dimer levels indicated that coagulation and fibrinolysis are activated in the patients with CU. Evaluation of platelet function may contribute to identify the role of these cells in the pathogenesis of CU.
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