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Background: Activated normal platelets undergo many biochemical and morphological changes, some of which are apoptotic. Platelet derived microparticles and shrinked platelets as hallmark of platelet activation and apoptosis disperse surfaces containing procoagulant activity around injured vessels and tissues. This study was conducted to determine microparticles formation and platelet shrinkage in Glanzmann thrombasthenia upon activation. Patients and Methods: Platelets from twelve unrelated type I Glanzmann thrombasthenia patients were examined as washed platelets. Calcium ionophore A23187 was used as agonist to activate the platelets. Flow cytometry was applied to measure platelet-derived micro particles (forward scatter events <1.0 µm size), and platelet shrinkage (mean-FSC). Anti-CD42b was used as platelet specific marker to distinguish platelets from other likely particles. Annexin A5 Alexa Fluor was used to determine phosphatidylserine exposure and confirm platelet activation and apoptosis. Results: Calcium ionophore A23187, dramatically increased MP formation by type-I GT platelets up to 14.5 fold increase over baseline (Buffer treated: 14.18 ± 5.4% vs. A23187 treated: 34.31 ± 15.2% p<0.005). Also calcium ionophore A23187, increased platelet shrinkage by type-I GT platelets and mean-FSC decreased (Buffer treated: 4.12±1.3 vs. A23187 treated: 1.67±0.2 p<0.0024). Conclusion: This study showed that, type I Glanzmann thrombasthenia platelets demonstrate platelet apoptosis considering two apoptotic targets, including micro particles formation and platelet shrinkage. We conclude that in thrombasthenic Glanzmann platelets at least some aspects of normal apoptosis is ongoing, and this may explain normal platelet count among these patients. Keywords: Apoptosis, Glanzmann thrombasthenia, glycoprotein IIbIIIa, flow cytometry, microparticle.

Keywords: Apoptosis, Glanzmann thrombasthenia, glycoprotein IIbIIIa, flow cytometry, microparticle

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