title: Glycoprotein IIIA gene (PlA) polymorphism and aspirin resistance: is there any correlation?
abstract: BACKGROUND
  Platelet glycoprotein (GP) IIb/IIIa receptors play an inevitable role in platelet aggregation. The GP IIIa gene is polymorphic (PlA1/PlA2) and the presence of a PlA2 allele might be associated with an increased risk for acute coronary syndrome (ACS).
  
  
  OBJECTIVE
  To examine the prevalence of the PlA2 allele in patients with ACS and in subjects with or without aspirin resistance.
  
  
  METHODS
  The prevalence of the PlA2 allele was assessed in 158 patients with ACS and PlA2 compared with its prevalence in 199 healthy volunteers. The antiplatelet efficacy of aspirin was examined in all patients with ACS, as well as in 69 individuals who had suffered ischemic stroke and in 58 high-risk subjects without any known ischemic vascular events.
  
  
  RESULTS
  PlA2 prevalence was significantly higher in patients with ACS (59/158) than in the control group (51/199; p < 0.05). Carriers of the PlA2 allele had a significantly higher risk of developing ACS, even after an adjustment to the risk factors (OR 5.74; 95% CI 1.75 to 18.8; p = 0.004). The occurrence of the PlA2 allele was significantly higher among patients with aspirin resistance than in subjects who demonstrated an appropriate response to the drug (allele frequencies, 0.21 vs 0.14; p < 0.05). All patients homozygous for the PlA2 allele had an inadequate platelet response to aspirin.
  
  
  CONCLUSIONS
  Our results support the hypothesis that carriers of the PlA2 allele might have an increased risk for ACS. PlA2 homozygosity was associated with an inadequate response to aspirin therapy. Our data further suggest that patients with PlA2 allele homozygosity might benefit from antiplatelet therapy based on adenosine diphosphate antagonists throughout secondary treatment for prevention of ACS.
authors.affiliation: First Department of Medicine, School of Medicine, University of Pecs, Pecs, Hungary. elod.papp@aok.pte.hu
authors.forename: Elod
authors.initials: E
authors.lastname: Papp
authors.forename: Viktoria
authors.initials: V
authors.lastname: Havasi
authors.forename: Judit
authors.initials: J
authors.lastname: Bene
authors.forename: Katalin
authors.initials: K
authors.lastname: Komlosi
authors.forename: Laszlo
authors.initials: L
authors.lastname: Czopf
authors.forename: Eva
authors.initials: E
authors.lastname: Magyar
authors.forename: Csaba
authors.initials: C
authors.lastname: Feher
authors.forename: Gergely
authors.initials: G
authors.lastname: Feher
authors.forename: Beata
authors.initials: B
authors.lastname: Horvath
authors.forename: Zsolt
authors.initials: Z
authors.lastname: Marton
authors.forename: Tamas
authors.initials: T
authors.lastname: Alexy
authors.forename: Tamas
authors.initials: T
authors.lastname: Habon
authors.forename: Levente
authors.initials: L
authors.lastname: Szabo
authors.forename: Kalman
authors.initials: K
authors.lastname: Toth
authors.forename: Bela
authors.initials: B
authors.lastname: Melegh
mesh_terms: D000328:Adult; D000368:Aged; D000483:Alleles; D001241:Aspirin / Q000494:pharmacology / Q000627:therapeutic use*; D004351:Drug Resistance; D050171:Dyslipidemias / Q000150:complications; D005260:Female; D005787:Gene Frequency; D005838:Genotype; D006801:Humans; D006814:Hungary; D006973:Hypertension / Q000150:complications; D039661:Integrin beta3 / Q000235:genetics*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000150:complications / Q000188:drug therapy* / Q000235:genetics; D009765:Obesity / Q000150:complications; D010979:Platelet Function Tests; D011110:Polymorphism, Genetic; D012307:Risk Factors; D012907:Smoking; D013577:Syndrome
chemical_list: D039661:Integrin beta3; D001241:Aspirin