Key result
Aspirin withdrawal in thrombocythaemia is linked to microvascular thrombosis preceded by a ~30-fold thromboxane increase.
Why the study?
The pathogenesis of arterial thrombotic events in patients with polycythaemia vera and essential thrombocythaemia is not clearly understood but may involve platelet function abnormalities and increased thromboxane formation.
Does low-dose aspirin inhibit platelet thromboxane formation and prevent arterial microvascular thrombosis in patients with thrombocythaemia?
Comparison
Withdrawal of aspirin followed by reinstitution of low-dose aspirin vs patients who remained asymptomatic
Design
Prospective cohort study
Follow-up
10 days after aspirin withdrawal
Authors
Loading...
Platelet thromboxane surge precedes microvascular thrombosis in ET/PV; supports aspirin use but hypothesis-generating pending larger trials.
Does low-dose aspirin inhibit platelet thromboxane formation and prevent arterial microvascular thrombosis in patients with thrombocythaemia?
In patients with thrombocythaemia, increased platelet thromboxane formation precedes arterial microvascular thrombosis, providing a mechanistic rationale for low-dose aspirin therapy.
Genderen et al. (1999) studied Polycythaemia vera (PV) and essential thrombocythaemia (ET) (n=7). Low-dose aspirin vs. Aspirin withdrawal was evaluated on Arterial microvascular thrombosis of extremities (erythromelalgia) and urinary thromboxane excretion. In patients with thrombocythaemia, arterial microvascular thrombosis following aspirin withdrawal was preceded by a 3-30-fold increase in urinary thromboxane excretion.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: