Journal
THROMBOSIS AND HAEMOSTASIS
Volume 112, Issue 1, Pages 118-127Publisher
GEORG THIEME VERLAG KG
DOI: 10.1160/TH13-10-0844
Keywords
Aspirin; prostacyclin; essential thrombocythaemia; platelets; thromboxane
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Funding
- Italian Ministry of Health (Ricerca Corrente) [BIO 03 2012]
- Catholic University [Linea D1-2012]
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Essential thrombocythaemia (ET) is characterised by enhanced platelet generation and thrombosis. Once daily (od) aspirin incompletely inhibits platelet thromboxane (TX)A(2) production in ET. A twice daily (bid) dosing is necessary to fully inhibit TXA(2). Whether this dosing regimen affects in vivo prostacyclin (PGI(2)) biosynthesis is unknown. PGI(2) biosynthesis was characterised in 50 ET patients on enteric-coated (EC) aspirin 100 mg od, by measuring its urinary metabolite, 2,3-dinor-6-keto-PGF(1 alpha) (PGI-M). Moreover, in a crossover study 22 patients poorly responsive to standard aspirin based on serum TXB2 levels (>= 4 ng/ml) were randomised to different seven-day aspirin regimens: EC aspirin 100 mg od, 100 mg bid, 200 mg od, or plain as-pirin 100 mg od. PGI-M measured 24 hours after the last aspirin intake (EC, 100 mg od) was similar in patients and healthy subjects both on (n=10) and off (n=30) aspirin. PGI-M was unrelated to in vivo TXA(2) biosynthesis, and not affected by EC aspirin 100 mg bid or 200 mg od as compared to EC 100 mg od. PGI(2) biosynthesis in aspirin-treated ET patients appears unrelated to TXA(2) biosynthesis, and not affected by an improved aspirin regimen, demonstrating its vascular safety for future trials.
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