It has been suggested that platelet hyperreactivity in patients with diabetes mellitus is associated with increased platelet production of thromboxane. We therefore compared the excretion of a thromboxane metabolite and platelet function in 50 patients with Type II diabetes mellitus who had normal renal function and clinical evidence of macrovascular disease and in 32 healthy controls.

The mean (±SD) excretion rate of urinary 11-dehydro-thromboxane B₂ was significantly higher in the patients than in the controls (5.94±3.68 vs. 1.50±0.79 nmol per day; P<0.001), irrespective of the type of macrovascular complication. Tight metabolic control achieved with insulin therapy reduced the levels of 11-dehydro-thromboxane B₂ by approximately 50 percent. The fractional conversion of exogenous thromboxane B₂ (infused at a rate of 4.5,45.3, or 226.4 fmol per kilogram of body weight per second) to urinary 11-dehydro-thromboxane B₂ was assessed in four patients, in whom it averaged 5.4±0.1 percent; this value did not differ from that measured in healthy subjects. Aspirin in low doses (50 mg per day for seven days) reduced urinary excretion of the metabolite by approximately 80 percent in four patients. The fact that thromboxane biosynthesis recovered over the following 10 days was consistent with a platelet origin of the urinary metabolite.

We conclude that in Type II diabetes (1) increased 11-dehydro-thromboxane B₂ excretion reflects enhanced biosynthesis of thromboxane A₂ by platelets rather than a shift in its metabolic disposition; (2) this is likely to reflect in vivo platelet activation; and (3) improved metabolic control as well as low-dose aspirin therapy may correct these abnormalities in platelet function to a variable extent. (N Engl J Med 1990; 322:1769–74.)