title: Differential effect of aspirin on platelet aggregation in IDDM.
abstract: Diabetes mellitus is associated with a high incidence of cardiovascular diseases not directly attributable to hyperlipidemia, smoking, or hypertension, but which in part may be explained by an enhanced tendency to thrombosis due to increased platelet activity. The aim of this study was to evaluate platelet function and compare the effectiveness of the antiplatelet drug aspirin on platelet aggregation in diabetic and nondiabetic subjects. Platelet aggregation and composition were examined in 20 male insulin-dependent diabetes mellitus (IDDM) patients and 20 nondiabetic control subjects matched for age and body mass index. All were normotensive with serum total cholesterol less than 6.5 mM. Although within the clinically acceptable normal range, blood pressure was significantly higher in diabetic patients (130/75 mmHg) than in control subjects (123/70 mmHg) (P less than 0.05). Serum thromboxane B2 and ex vivo aggregation of platelets in response to two doses of the agonists collagen and platelet-activating factor (PAF) were similar to nondiabetic subjects. However, after taking 100 mg/day aspirin for 5 days, platelet aggregation to collagen was reduced by 76% in control subjects compared to 56% in IDDM patients (P less than 0.001). Aspirin treatment also reduced the slope of the aggregation curve and increased the lag time (the period between the addition of collagen and the start of irreversible aggregation) significantly more in control than in diabetic platelets. This difference in platelet aggregation could not be attributed to differences in platelet serotonin or thromboxane A2 secretion, the latter being almost completely suppressed by aspirin in each group. Platelet aggregation to PAF was similar in both groups and was not affected by aspirin.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Medicine, University of Western Australia, Royal Perth Hospital, Perth.
authors.forename: T A
authors.initials: TA
authors.lastname: Mori
authors.forename: R
authors.initials: R
authors.lastname: Vandongen
authors.forename: A J
authors.initials: AJ
authors.lastname: Douglas
authors.forename: R K
authors.initials: RK
authors.lastname: McCulloch
authors.forename: V
authors.initials: V
authors.lastname: Burke
mesh_terms: D000328:Adult; D001241:Aspirin / Q000494:pharmacology*; D001794:Blood Pressure; D002784:Cholesterol / Q000097:blood; D003094:Collagen / Q000494:pharmacology; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000503:physiopathology; D015525:Fatty Acids, Omega-3 / Q000097:blood; D006801:Humans; D019787:Linoleic Acid; D008041:Linoleic Acids / Q000097:blood; D008297:Male; D008560:Membrane Fluidity / Q000187:drug effects; D010743:Phospholipids / Q000097:blood; D010972:Platelet Activating Factor / Q000494:pharmacology; D010974:Platelet Aggregation / Q000187:drug effects*; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D012016:Reference Values; D013929:Thromboxane B2 / Q000097:blood
chemical_list: D015525:Fatty Acids, Omega-3; D008041:Linoleic Acids; D010743:Phospholipids; D010972:Platelet Activating Factor; D010975:Platelet Aggregation Inhibitors; D013929:Thromboxane B2; D003094:Collagen; D002784:Cholesterol; D019787:Linoleic Acid; D001241:Aspirin