title: Does high serum uric acid level cause aspirin resistance?
abstract: In patients with coronary artery disease (CAD), though aspirin inhibits platelet activation and reduces atherothrombotic complications, it does not always sufficiently inhibit platelet function, thereby causing a clinical situation known as aspirin resistance. As hyperuricemia activates platelet turnover, aspirin resistance may be specifically induced by increased serum uric acid (SUA) levels. In this study, we thus investigated the association between SUA level and aspirin resistance in patients with CAD. We analyzed 245 consecutive patients with stable angina pectoris (SAP) who in coronary angiography showed more than 50% occlusion in a major coronary artery. According to aspirin resistance, two groups were formed: the aspirin resistance group (Group 1) and the aspirin-sensitive group (Group 2). Compared with those of Group 2, patients with aspirin resistance exhibited significantly higher white blood cell counts, neutrophil counts, neutrophil-to-lymphocyte ratios, SUA levels, high-sensitivity C-reactive protein levels, and fasting blood glucose levels. After multivariate analysis, a high level of SUA emerged as an independent predictor of aspirin resistance. The receiver-operating characteristic analysis provided a cutoff value of 6.45 mg/dl for SUA to predict aspirin resistance with 79% sensitivity and 65% specificity. Hyperuricemia may cause aspirin resistance in patients with CAD and high SUA levels may indicate aspirin-resistant patients. Such levels should thus recommend avoiding heart attack and stroke by adjusting aspirin dosage.
authors.affiliation: aDepartment of Cardiology, Pamukkale University, DenizlibIzmir Ataturk Training and Research HospitalcIzmir Bozyaka Training and Research Hospital, IzmirdDepartment of Cardiology, Diskapi Training and Research Hospital, AnkaraeDepartment of Public Health, Pamukkale University, Denizli, Turkey.
authors.forename: Bekir S
authors.initials: BS
authors.lastname: Yildiz
authors.forename: Emel
authors.initials: E
authors.lastname: Ozkan
authors.forename: Fatma
authors.initials: F
authors.lastname: Esin
authors.forename: Yusuf I
authors.initials: YI
authors.lastname: Alihanoglu
authors.forename: Hayrettin
authors.initials: H
authors.lastname: Ozkan
authors.forename: Murat
authors.initials: M
authors.lastname: Bilgin
authors.forename: Ismail D
authors.initials: ID
authors.lastname: Kilic
authors.forename: Ahmet
authors.initials: A
authors.lastname: Ergin
authors.forename: Havane A
authors.initials: HA
authors.lastname: Kaftan
authors.forename: Harun
authors.initials: H
authors.lastname: Evrengul
mesh_terms: D000368:Aged; D000787:Angina Pectoris / Q000097:blood / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy*; D001241:Aspirin / Q000627:therapeutic use*; D015415:Biomarkers; D001772:Blood Cell Count; D001786:Blood Glucose / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism; D003324:Coronary Artery Disease / Q000097:blood / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy*; D054796:Drug Dosage Calculations; D004351:Drug Resistance; D005260:Female; D006801:Humans; D033461:Hyperuricemia / Q000097:blood / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy*; D008214:Lymphocytes / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000378:metabolism / Q000473:pathology; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D012372:ROC Curve; D012680:Sensitivity and Specificity; D014527:Uric Acid / Q000097:blood*
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D010975:Platelet Aggregation Inhibitors; D014527:Uric Acid; D002097:C-Reactive Protein; D001241:Aspirin