Genetic determined low response to thienopyridines is associated with higher systemic inflammation in smokers.
Fiche publication
Date publication
avril 2015
Auteurs
Membres identifiés du Cancéropôle Est :
Dr VISVIKIS Sophie
Tous les auteurs :
Shahabi P, Cuisset T, Stathopoulou MG, Morange PE, Grosdidier C, Herbeth B, Siest G, Alessi MC, Visvikis-Siest S
Lien Pubmed
Résumé
AIM: To investigate whether the interactions of CYP2C19*2 and CYP2C19*17 with smoking are associated with the levels of P2Y12 receptor inhibition and CRP, in on-thienopyridine post-stenting patients. METHODS & RESULTS: At 1-month follow-up, the interactions of smoking and CYP2C19 polymorphisms on the vasodilator-stimulated phosphoprotein - platelet reactivity index (VASP PRI), and CRP were explored in three metabolizing groups (1128 patients) as follow: poor metabolizers (*2 carriers/*17 noncarriers); intermediate metabolizers (*2 carriers/*17 carriers or *2 noncarriers/*17 noncarriers); and ultrarapidmetabolizers (*2 allele noncarriers/*17 carriers). The interactions of metabolizing status and smoking was significant for CRP (p = 0.001) but not for VASP PRI (p = 0.734). CONCLUSION: Interaction between CYP2C19 polymorphisms and smoking modifies on-treatment CRP level of post-stenting, on-thienopyridine patients. This effect seems to be independent to the level of P2Y12 receptor inhibition. Original submitted 1 August 2014; Revision submitted 4 February 2015.
Référence
Pharmacogenomics. 2015 Apr;16(5):459-69