Why the study?
How does platelet aggregation in whole blood compare to platelet-rich plasma in patients with Glanzmann's thrombasthenia?
How does platelet aggregation in whole blood compare to platelet-rich plasma in patients with Glanzmann's thrombasthenia?
The abnormality in Glanzmann's thrombasthenia may lie in the inability to form large macroscopic aggregates rather than a complete failure of platelet aggregation.
Challenges reliance on PRP aggregometry alone in Glanzmann's thrombasthenia; case report leaves open impact on bleeding risk assessment.
We examined platelet aggregation in platelet-rich plasma (PRP) and in whole blood from two patients with Glanzmann's thrombasthenia. In PRP, aggregation was measured by monitoring the changes in light absorbance that occurred in response to aggregating agents; to measure platelet aggregation in whole blood, we used a platelet counting technique. In PRP, the patients' platelets showed defective aggregation in response to ADP, adrenaline, arachidonic acid (AA), and collagen, but normal agglutination occurred in response to ristocetin. In whole blood, however, platelet aggregation in response to the aggregating agents appeared to be either very similar to that which occurred in blood from normal subjects or only slightly reduced. There was a reduced response to all concentrations of ADP and to low concentrations of collagen but a normal response to all concentrations of adrenaline, AA, and higher concentrations of collagen. Conversely, there seemed to be an increased agglutination response to ristocetin. The abnormality in our two patients with Glanzmann's thrombasthenia probably lies in the inability of their platelets to form large, macroscopic aggregates rather than in platelet aggregation per se.
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Burgess-Wilson et al. (1987) studied this question.
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