Patients with diabetes mellitus are several fold more prone to various forms of vascular diseases than are the non-diabetic subjects. Because platelets are in the key position in thrombus formation and possibly in atherogenesis, much interest has focused on the role of platelets in the development of diabetic vascular disease. Most studies on this topic have suggested increased adhesiveness and aggregability of the platelets from diabetic patients. The increased production of von Willebrand factor may account for the enhanced adhesion. The shift of the balance between proaggregatory thromboxane A2 and antiaggregatory prostacyclin to the dominance of thromboxane A2 could explain the increased aggregability of diabetic platelets, but the data available at the moment do not allow the conclusion that such a change really exist in human in vivo. One recent work has suggested that the increased glycosylation of connective tissue proteins in diabetes would increase their aggregating potency, but also this finding needs further confirmation.