ArticleArchives of medical science : AMS2018
Glycoprotein Ibα Kozak polymorphism in patients presenting with early-onset acute coronary syndrome.
Article in Archives of medical science : AMS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
introductionGlycoprotein Ibα (GPIbα) receptor is the chief molecule responsible for initial platelet adhesion to the subendothelium. A thymidine to cytosine single nucleotide substitution at position -5 from the ATG start codon characterizes the Kozak sequence polymorphism. The Kozak sequence polymorphism may increase the surface expression of GPIbα and contribute to thrombogenesis. We evaluated the allele frequencies of GPIbα Kozak sequence polymorphism in the Turkish population and examined the relationship between GPIbα Kozak sequence polymorphism and early-onset acute coronary syndrome (ACS). MATERIAL AND
methodsThis study enrolled 200 patients (122 male, 78 female, mean age: 39 ±5 years) and 200 healthy control subjects (110 male, 90 female, 41 ±4 years). The patient group was composed of patients admitted to our coronary care unit with early-onset ACS and patients who attended to our cardiology outpatient clinic after hospital discharge with a diagnosis of early-onset ACS.
resultsKozak polymorphism frequencies in patients and control subjects did not differ significantly (23% versus 22.5%,
conclusionsAlthough the frequency of GPIbα Kozak polymorphism did not differ significantly in early-onset ACS patients versus control subjects, Kozak polymorphism frequency was borderline significantly higher in patients who presented with NSTEMI when compared to patients with STEMI.
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