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

Caterina Pettinella1, Mario Romano, Liborio Stuppia

  • 1Center of Excellence on Aging, 'G. d'Annunzio' University Foundation, Chieti, Italy.

Thrombosis and Haemostasis
|April 8, 2009
PubMed

Insights

The C50T/A-842G COX-1 gene haplotype does not influence aspirin

Area of Science:

  • Pharmacogenomics
  • Cardiovascular Research
  • Molecular Biology

Background:

  • Cyclooxygenase-1 (COX-1) gene polymorphisms, specifically C50T and A-842G, are investigated for their role in aspirin response.
  • Previous studies suggest these polymorphisms may affect aspirin's pharmacological efficacy, but evidence remains controversial.
  • Understanding these genetic factors is crucial for personalized antiplatelet therapy.

Purpose of the Study:

  • To investigate the association between the C50T/A-842G COX-1 haplotype and the antiplatelet response to low-dose aspirin.
  • To determine if these polymorphisms influence aspirin resistance in healthy individuals.
  • To evaluate the thromboxane-dependence of aspirin's antiplatelet effects in relation to this haplotype.

Main Methods:

  • Genotyping of 148 healthy individuals for the C50T/A-842G haplotype.
  • Low-dose aspirin (100 mg daily) treatment for 30 individuals over four weeks.
  • Monitoring of serum thromboxane B(2), urinary 11-dehydro-TXB(2), and arachidonic acid-induced platelet aggregation.

Main Results:

  • The C50T/A-842G haplotype was present in 6.7% of subjects (heterozygous) and 0.67% (homozygous).
  • Low-dose aspirin suppressed platelet aggregation and thromboxane levels similarly in both carriers and non-carriers of the haplotype.
  • No correlation was found between the C50T/A-842G haplotype and aspirin resistance.

Conclusions:

  • The C50T/A-842G COX-1 gene haplotype does not appear to be a significant determinant of response to low-dose aspirin therapy.
  • Platelet cyclooxygenase activity is uniformly suppressed by low-dose aspirin, irrespective of the presence of these specific polymorphisms.
  • These findings suggest that genetic variations in COX-1 at these loci may not be a primary driver of aspirin resistance.

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