Cyclooxygenase-1 haplotype C50T/A-842G does not affect platelet response to aspirin

Caterina Pettinella; Mario Romano; Liborio Stuppia; Francesca Santilli; Rossella Liani; Giovanni Davì

doi:10.1160/TH08-11-0753

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 2009; 101(04): 687-690
DOI: 10.1160/TH08-11-0753

Rapid and Short Communication

Schattauer GmbH

Cyclooxygenase-1 haplotype C50T/A-842G does not affect platelet response to aspirin

Authors

Caterina Pettinella

¹Center of Excellence on Aging, “G. d’Annunzio” University Foundation, Chieti, Italy
Mario Romano

¹Center of Excellence on Aging, “G. d’Annunzio” University Foundation, Chieti, Italy
Liborio Stuppia

¹Center of Excellence on Aging, “G. d’Annunzio” University Foundation, Chieti, Italy
Francesca Santilli

¹Center of Excellence on Aging, “G. d’Annunzio” University Foundation, Chieti, Italy
Rossella Liani

¹Center of Excellence on Aging, “G. d’Annunzio” University Foundation, Chieti, Italy
Giovanni Davì

¹Center of Excellence on Aging, “G. d’Annunzio” University Foundation, Chieti, Italy

Abstract

Summary

COX-1 polymorphism C50T, in complete linkage disequilibrium with the other polymorphism A-842G, has been depicted as a determinant of pharmacological response to aspirin treatment. Whether these polymorphisms exert an effect on response to aspirin both in vitro and ex vivo is still controversial. We geno-typed a population of 148 healthy individuals for the C50T/A-842G haplotype. Thirty of them underwent low-dose aspirin (100 mg daily) treatment for four weeks and were followed up for seven days after withdrawal. In this subgroup, we evaluated the thromboxane-dependence of biochemical and functional indexes used to monitor the antiplatelet effect of low-dose aspirin. Among the 148 subjects studied, 10 were heterozygous for the C50T/A-842G haplotype (6.7%) and only one was homozygous for the 50T/-842G haplotype (0.67%). In the group on low-dose aspirin, serum thromboxane (TX) B₂ as well as urinary 11-dehydro-TXB₂ and arachidonic acid (AA)-induced aggregation were similarly suppressed in carriers and non-carriers of the 50T/-842G haplotype, with an increase until basal levels of all the parameters within seven days after withdrawal. We found no relationship between the 50T/-842G haplotype and the so-called phenomenon of aspirin resistance. Platelet cyclooxygenase activity, as reflected by serum TXB₂, was uniformly and persistently suppressed by low-dose aspirin in both carriers and non carriers of these polymorphisms.

Keywords

Aspirin resistance - polymorphisms - pharmacogenetics

Full Text

References

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