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KMID : 0377519930180010075
Chung-Ang Journal of Medicine
1993 Volume.18 No. 1 p.75 ~ p.86
Effect of Aspirin on Platelet Aggregation in Patients with Non-Obese Non-Insulin-Dependent Diabetes Mellitus




Abstract
Diabetes mellitus is an independent risk factor of cardiovascular disease in addition to hyperlipidemia, smoking or hypertension. The association of diabetes mellitus with a high incidence of cardiovascular disease is not entirely attributable to
hyperlipidemia, smoking or hypertension, but which in part may be explained by an enhanced tendency to thrombosis due to increased platelet activity. many previous reports have indicated that platelet aggregation may be increased in platelet
aggregation
in patients with non-insulin-dependent diabetes mellitus(NIDDM) was rarely reported. The aim of this study was to evaluate platelet function and compared the effectiveness of antiplatelet drug, aspirin, on platelet aggregation in patients with
nonobese
NIDDM and nondiabetic control subjects.
Platelet aggregation were examined in 20 male patients with non-obese NIDDM and 20 nondiabetic control subjects matched for age and body mass index. All were normotensive with serum total cholesterol concentration less than 250 mg/§¢.
Platelet aggregation of diabetic patients in response to two doses of agonists, collagen and platelet activating factor(PAF0 were similar to those of nondiabetic control subjects. Nevertheless, after taking aspirin 100mg daily for 7 days,
platelet
aggregation to collagen was inhibited by 78% in control subjects compared to 53% in patients with non-obese NIDDM(p<0.001). aspirin treatment also reduced the slope of the platelet aggregation curve and increased the lag time significantly in
control
subjects compared to patients with non-obese NIDDM.
This difference in platelet aggregation could not be attributed to differences in platelet serotonin or thromboxane B2 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.
This results suggest that platelet from patients with non-obese NIDDM are resistant to the effect of aspirin by mechanism independent of both the cyclooxygenase and platelet activating factor pathways of aggregation, and short-term low dose
aspirin
is
less effective for prevention of cardiovascular complication in patients with non-obese NIDDM.
KEYWORD
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