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Platelet thromboxane synthesizing activity in non-insulin-dependent diabetes: correlation with diabetic retinopathy
Abstract:
Since elevated thromboxane A2 synthesis could be expected to lead to microvascular injury in diabetic patients, it is important to determine the relationship between thromboxane A2 synthesis and diabetic microvascular complications. In the present study, the activity of thromboxane A2 synthesis in platelets was assessed in 57 Type 2 (non-insulin-dependent) diabetic patients by measuring the conversion of exogenously added 14C-arachidonic acid into 14C-thromboxane B2. The activity of thromboxane synthesis was significantly higher in diabetic patients than in 16 age-matched control subjects (2.61 +/- 0.07 vs 1.95 +/- 0.12 microgram . 10(9) platelets-1 . 3 min-1, respectively, p less than 0.001). When the diabetic patients were divided into three groups (nil, background, and proliferative retinopathy) on the basis of severity of diabetic retinopathy, there was a trend to increased thromboxane synthesizing activity as diabetic retinopathy develops. However, no statistically significant changes were demonstrated among these three groups. In the diabetic patients, a positive correlation was found between thromboxane synthesizing activities and glycosylated hemoglobin values (biochemical indicator of long-term glycemic control), but not between the activities and plasma glucose levels. To ascertain the effect of desirable diabetic treatment on thromboxane synthesizing activity in platelets, 9 newly diagnosed patients and 6 poorly controlled patients were examined. During treatment, all patients had declining plasma glucose and glycosylated hemoglobin levels. Thromboxane synthesizing activities in 6 patients treated by insulin decreased significantly during treatment (3.16 +/- 0.17 to 2.49 +/- 0.22 microgram . 10(9) platelets-1 .3 min-1, p less than 0.01), but 9 diabetic patients treated by diet or sulphonylureas still maintained their elevated thromboxane synthesizing activity levels (2.76 +/- 0.24 to 2.66 +/- 0.25 microgram . 10(9) platelets-1 .3 min-1,NS). These results suggest that the increased thromboxane synthesizing enzyme system is involved in the abnormal platelet function in diabetes independently of diabetic retinopathy, and that appropriate metabolic control using insulin might be successful in lowering the increased thromboxane synthesizing activity.