Key result
PGE2 potentiation of LASS-induced platelet aggregation was markedly diminished in patients with storage pool disease, but remained normal after aspirin ingestion.
Why the study?
Does PGE2 potentiation of LASS-induced platelet aggregation differ between patients with storage pool disease and normal subjects after aspirin ingestion?
Population
6 patients with storage pool disease and normal subjects
Comparison
In vitro exposure to LASS and prostaglandin E2 vs Normal subjects after aspirin ingestion
Design
Preclinical
Authors
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Suggests distinct PGE2 pathways in storage pool disease; leaves open clinical translation to antiplatelet strategies.
Observational (n=6)
Does PGE2 potentiation of LASS-induced platelet aggregation differ between patients with storage pool disease and normal subjects after aspirin ingestion?
The study elucidates the mechanism of irreversible platelet aggregation, showing that aspirin blocks LASS/PGE2 production while storage pool disease impairs the response to PGE2 potentiation.
Weiss et al. (1976) conducted an observational in Storage pool disease (n=6). Storage pool disease and aspirin ingestion vs. Normal platelets was evaluated on Potentiation of LASS-induced platelet aggregation by PGE2. PGE2 potentiation of LASS-induced platelet aggregation was markedly diminished in patients with storage pool disease, but remained normal after aspirin ingestion.
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