title: Aspirin resistance in cerebrovascular disease and the role of glycoprotein IIIa polymorphism in Turkish stroke patients.
abstract: Aspirin resistance occurs in 5-45% of high-risk patients, with various mechanisms proposed for its development. This study aimed to determine the relationships among aspirin resistance, aspirin dosage, type of aspirin and glycoprotein IIIa P1A1/A2 polymorphism in patients with vascular risk factors. Two hundred and eight (75 symptomatic, 133 asymptomatic) patients with vascular risk factors who were using aspirin for primary or secondary prevention were prospectively included. The symptomatic group was further classified into two groups according to aspirin use at the time of stroke. Aspirin resistance was measured by the PFA-100 system (collagen/epinephrine cartridge) and glycoprotein IIIa P1A1/A2 polymorphism was determined by PCR. The overall prevalence of aspirin resistance was 32.2%. The mean age of patients with aspirin resistance was significantly higher than that in those who did not have resistance (P = 0.009). The prevalence of aspirin resistance was similar for the symptomatic and asymptomatic under aspirin therapy groups. The resistance rate was found to be highest with 100 mg enteric-coated preparation use (39.3%). Increasing the aspirin dosage and/or shifting to uncoated preparations caused a change in aspirin sensitivity of 36-60%. Repeated measurements showed development of aspirin resistance in 14% of patients who were sensitive to aspirin in previous measurements. Glycoprotein IIIaP1A1/A2 polymorphism, aspirin resistance and development of atherothrombotic stroke were not significantly related. The effect of aspirin can change by time, dosage and type of preparation used. There are no relationships among glycoprotein IIIa P1A1/A2 polymorphism, aspirin resistance and development of atherothrombotic stroke.
authors.affiliation: aDepartment of Neurology bDepartment of Biochemistry cDepartment of Medical Biology and Genetics, School of Medicine, Baskent University, Ankara, Turkey.
authors.forename: Eda
authors.initials: E
authors.lastname: Derle
authors.forename: Ruhsen
authors.initials: R
authors.lastname: Öcal
authors.forename: Seda
authors.initials: S
authors.lastname: Kibaroğlu
authors.forename: Ceyda
authors.initials: C
authors.lastname: Çelikkol
authors.forename: Nilüfer
authors.initials: N
authors.lastname: Bayraktar
authors.forename: Hasibe
authors.initials: H
authors.lastname: Verdi
authors.forename: Belgin F
authors.initials: BF
authors.lastname: Ataç
authors.forename: Ufuk
authors.initials: U
authors.lastname: Can
mesh_terms: D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D001241:Aspirin / Q000627:therapeutic use*; D058070:Asymptomatic Diseases; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D004351:Drug Resistance; D005260:Female; D015870:Gene Expression; D006801:Humans; D039661:Integrin beta3 / Q000235:genetics* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D011110:Polymorphism, Genetic; D055502:Secondary Prevention; D012720:Severity of Illness Index; D020521:Stroke / Q000150:complications / Q000235:genetics / Q000473:pathology / Q000517:prevention & control*; D013927:Thrombosis / Q000150:complications / Q000235:genetics / Q000473:pathology / Q000517:prevention & control*
chemical_list: D039661:Integrin beta3; D010975:Platelet Aggregation Inhibitors; D001241:Aspirin