title: Aspirin resistance is associated with glycemic control, the dose of aspirin, and obesity in type 2 diabetes mellitus.
abstract: OBJECTIVE
  Aspirin resistance (AR) is increased in diabetic patients. It is not known whether glycemic control has effect on AR.
  
  
  METHODS
  To test the hypothesis that glycemic control might have influence on aspirin resistance, we measured aspirin resistance and glycated hemoglobin (HbA1c) in diabetic patients. We also measured aspirin resistance in nondiabetic subjects and compared the results with the diabetic group.
  
  
  METHODS
  We examined AR in 108 diabetic patients and 67 nondiabetic subjects with impedance platelet aggregometry. Glycemic control was evaluated according to both fasting blood glucose (FBG) and HbA1c levels.
  
  
  RESULTS
  According to the analyses, diabetic patients had significantly higher AR (P < 0.01), alanine aminotransferase (P < 0.005), and body mass index (P < 0.05) and significantly lower high-density lipoprotein cholesterol (P < 0.005) levels compared with nondiabetic controls. A correlation analysis revealed that AR was positively correlated with body mass index (r = 0.190, P < 0.01), fasting blood glucose (r = 0.224, P < 0.001), and HbA1c levels (r = 0.297, P < .0001). Using low-dose aspirin (100 mg/d) was a risk factor for aspirin-resistant status in both diabetic patients (odds ratio 1.26, 95% confidence interval 1.01-1.58, P < 0.05) and overall study group (odds ratio 1.3, 95% confidence interval 1.08-1.56, P < 0.01).
  
  
  CONCLUSIONS
  These data suggest that glycemic control, obesity, and the dose of aspirin have influence on AR in diabetic subjects. Further studies with larger groups are needed to clarify the role of glycemic control on AR.
authors.affiliation: Department of Internal Medicine, Kecioren Research and Training Hospital, 06830 Ankara, Turkey. dertaner@gmail.com
authors.forename: Derun Taner
authors.initials: DT
authors.lastname: Ertugrul
authors.forename: Emre
authors.initials: E
authors.lastname: Tutal
authors.forename: Mehmet
authors.initials: M
authors.lastname: Yildiz
authors.forename: Okhan
authors.initials: O
authors.lastname: Akin
authors.forename: Ahmet Arif
authors.initials: AA
authors.lastname: Yalçin
authors.forename: Oznur Sari
authors.initials: OS
authors.lastname: Ure
authors.forename: Hamiyet
authors.initials: H
authors.lastname: Yilmaz
authors.forename: Bünyamin
authors.initials: B
authors.lastname: Yavuz
authors.forename: Onur Sinan
authors.initials: OS
authors.lastname: Deveci
authors.forename: Naim
authors.initials: N
authors.lastname: Ata
authors.forename: Metin
authors.initials: M
authors.lastname: Küçükazman
mesh_terms: D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D001241:Aspirin / Q000008:administration & dosage / Q000494:pharmacology*; D001786:Blood Glucose / Q000378:metabolism*; D015992:Body Mass Index; D008078:Cholesterol, LDL / Q000097:blood; D016001:Confidence Intervals; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000503:physiopathology*; D004351:Drug Resistance; D005260:Female; D006442:Glycated Hemoglobin / Q000378:metabolism; D006801:Humans; D016015:Logistic Models; D008297:Male; D009765:Obesity / Q000209:etiology / Q000503:physiopathology*; D016017:Odds Ratio; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000008:administration & dosage / Q000494:pharmacology*; D012307:Risk Factors
chemical_list: D000410:Alanine Transaminase; D001241:Aspirin; D001786:Blood Glucose; D008078:Cholesterol, LDL; D006442:Glycated Hemoglobin; D010975:Platelet Aggregation Inhibitors