ABSTRACT
It has been suggested that platelet hyper-reactivity in patients with diabetes mellitus [D.M.] is associated with increased platelet production of thromboxane. We therefore compared the excretion of thromboxane metabolite and platelet function in 30 patients with diabetes mellitus who had normal renal function and 18 healthy controls. The mean [ +/- SD] excretion rate of urinary 11-dehydro-thromboxane B2 was siginifcantly higher than in the controls [p<0.00/]. Aspirin in low doses [50 mg per day for 7 daye] reduced urinary excretion of the metabolite by approximately 80% in four patients. We concluded that in type l/ diabetes that [i], increased 11-dehydtro-thromboxane B2 excretion reflects enhanced biosynthesis of thromboxane A2 by platelets rather than a shift in its metabolic disposition [ii]. This is likely to reflect in Vivo platelet activation. [iii]. Improved metabolic control as well as low doses aspirin therapy may correct these abnormality in platelet function to a variable extent