Glycoprotein IIIA (PlA) polymorphism aspirin resistance: Is there any correlation?

E. Papp, V. Havasi, J. Bene, K. Komlósi, L. Czopf, Eva Magyar, Csaba Feher, G. Fehér, B. Horváth, Zsolt Marton, Tamas Alexy, Tamas Habon, Levente Szabo, K. Tóth, B. Melegh

Research output: Contribution to journalArticle

61 Citations (Scopus)

Abstract

BACKGROUND: Platelet glycopratein (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 Pl42 allele in patients with ACS and in subjects with or without aspirin resistance. METHODS: The prevalence of the Pl42 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% Cl 1.75 to 18.8; p = 0.004). The occurrence of the PIA2 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 PIA2 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.

Original languageEnglish
Pages (from-to)1013-1018
Number of pages6
JournalAnnals of Pharmacotherapy
Volume39
Issue number6
DOIs
Publication statusPublished - Jun 2005

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Acute Coronary Syndrome
Aspirin
Glycoproteins
Alleles
Blood Platelets
Secondary Prevention
Platelet Aggregation
Gene Frequency
Adenosine Diphosphate
Blood Vessels
Healthy Volunteers
Therapeutics
Stroke
Control Groups
Pharmaceutical Preparations
Genes

Keywords

  • Aspirin resistance
  • PlA polymorphism

ASJC Scopus subject areas

  • Pharmacology (medical)
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

Glycoprotein IIIA (PlA) polymorphism aspirin resistance : Is there any correlation? / Papp, E.; Havasi, V.; Bene, J.; Komlósi, K.; Czopf, L.; Magyar, Eva; Feher, Csaba; Fehér, G.; Horváth, B.; Marton, Zsolt; Alexy, Tamas; Habon, Tamas; Szabo, Levente; Tóth, K.; Melegh, B.

In: Annals of Pharmacotherapy, Vol. 39, No. 6, 06.2005, p. 1013-1018.

Research output: Contribution to journalArticle

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abstract = "BACKGROUND: Platelet glycopratein (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 Pl42 allele in patients with ACS and in subjects with or without aspirin resistance. METHODS: The prevalence of the Pl42 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{\%} Cl 1.75 to 18.8; p = 0.004). The occurrence of the PIA2 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 PIA2 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.",
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T1 - Glycoprotein IIIA (PlA) polymorphism aspirin resistance

T2 - Is there any correlation?

AU - Papp, E.

AU - Havasi, V.

AU - Bene, J.

AU - Komlósi, K.

AU - Czopf, L.

AU - Magyar, Eva

AU - Feher, Csaba

AU - Fehér, G.

AU - Horváth, B.

AU - Marton, Zsolt

AU - Alexy, Tamas

AU - Habon, Tamas

AU - Szabo, Levente

AU - Tóth, K.

AU - Melegh, B.

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N2 - BACKGROUND: Platelet glycopratein (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 Pl42 allele in patients with ACS and in subjects with or without aspirin resistance. METHODS: The prevalence of the Pl42 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% Cl 1.75 to 18.8; p = 0.004). The occurrence of the PIA2 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 PIA2 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.

AB - BACKGROUND: Platelet glycopratein (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 Pl42 allele in patients with ACS and in subjects with or without aspirin resistance. METHODS: The prevalence of the Pl42 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% Cl 1.75 to 18.8; p = 0.004). The occurrence of the PIA2 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 PIA2 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.

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