Platelet prothrombinase activity, a final pathway platelet procoagulant activity, is overexpressed in type 1 diabetes: No relationship with mean platelet volume or background retinopathy

There is overwhelming evidence that platelets from diabetic individuals are hyperreactive, not only when microvascular complications are apparent, but already at an early stage of the disease. There is still controversy about the question of whether primary hyperreactive platelets may contribute to the origin or progression of microangiopathy or whether diabetic platelet h yperfunctionality is just a logical consequence of a continuous low-grade a ctivation of platelets by contact with a diseased microvascular wall. As a consequence of platelet activation, the outer layer of its phospholipid mem brane is more procoagulant than in the quiescent state, stimulating thrombi n formation in plasma. This platelet function is called platelet procoagula nt activity. We studied platelet prothrombinase activity (PPA), a final pat hway platelet procoagulant activity of type 1 diabetic platelets, and looke d for an eventual correlation with microvascular disease (background retino pathy) and mean platelet volume (MPV). Stypven clotting times (SCTs), refle cting PPA expression, and MPV of citrated platelet-rich plasma (PRP), were measured in 21 patients with type 1 diabetes-10 with and 11 without backgro und retinopathy-under clinically acceptable metabolic control and compared them to 20 disease-free voluntary controls. We also compared PPA expression and MPV in diabetic individuals with and without retinopathy. With the SCT , a selective test adapted for studying PPA in PRP, we found hyper expressi on of PPA in all diabetic patients. We found no difference in MPV between d iabetic and control PRP. Comparing patients with and without background ret inopathy we found no significant difference in PPA expression. From these r esults, we suggest that the phospholipid surface of diabetic platelets, mor e than the surface of normal control platelets, stimulate the expression of PPA. This diabetic platelet coagulant anomaly was not related to an increa sed platelet mass (higher MPV) nor to the presence of microangiopathy. We c onclude that PPA hyperexpression is associated with patients with type 1 di abetes, already occurring in an early stage of the disease, and not necessa rily a consequence of early-stage microvascular disease, because the anomal y is also demonstrable, in the same degree, in patients with diabetes witho ut microangiopathy.