Aspirin Resistance Genetic Polymorphisms (PEAR1, PTGS1, GPIIIa) Detection Kit (Colloidal Gold)

Epidemiology

Aspirin, an effective inhibitor of platelet aggregation, is extensively used to prevent and treat cardiovascular and cerebrovascular diseases. Research reveals that a subset of patients, roughly 50–60%, develop aspirin resistance (AR), where long-term low-dose aspirin does not sufficiently inhibit platelet function; this resistance shows significant racial differences. The glycoprotein IIb/IIIa (GPIIb/IIIa) receptor is crucial for platelet aggregation and acute thrombus formation at vascular injury sites. Genetic polymorphisms, particularly in GPIIIa P1A1/A2, PEAR1, and PTGS1, are strongly implicated in AR. The GPIIIa P1A2 allele is a key contributor; its mutation alters GPIIb/IIIa structure, promoting cross-linking and aggregation. Aspirin-resistant patients have a higher frequency of the P1A2 allele, and those with P1A2/A2 homozygosity exhibit poor drug response. Stent patients with mutant P1A2 alleles face a subacute thrombotic event rate five times that of P1A1 homozygotes, often requiring higher aspirin doses for anticoagulation. Regarding PEAR1, individuals with the GG genotype respond well to aspirin, whereas AA or AG genotype patients taking aspirin (with or without clopidogrel) post-stent implantation have elevated risks of myocardial infarction and mortality. For PTGS1, the GG genotype carries a high risk of AR (HR: 10) and a high incidence of cardiovascular events (HR: 2.55); the AG genotype confers moderate risk, necessitating close monitoring of aspirin efficacy; the AA genotype is more sensitive, with a relatively low event rate. The results of this test reflect only the analysis of human PEAR1, PTGS1, and GPIIIa genes.

Work Flow

The process involves an automatic nucleic acid extractor. A sample volume of 200 μL is used for extraction, with a recommended elution volume of 100 μL.