HEPARIN-RELEASED PLATELET FACTOR 4 (HR-PF4) IN DIABETIC MICR0VAS-CULAR DISEASE
When heparin is injected i.v. as a bolus, PF4 but not (β-throm boglobulin ((βTG) is released immediately. HR-PF4 is not liberated from platelets but from the endothelial cells of vessels which serve as storage sites. The role of platelet activation in diabetic microvascular disease is still controversial, however there is experimental evidence of vascular injury and hemostatic activation preceding the appearance of microvascular disease. The contradictory results so far obtained in man may be partly attributed to the heterogeneity of the diabetic patients studied. We studied 20 insulin-dependent diabetics (age 21-40) in stable metabolic equilibrium (mean HbAlc=7.6%). 10 without fluoroangiographic evidence of retinopathy (Group l) and 10 with retinopathy (Group 2). None had signs or symptoms of macrovascular disease. The control group consisted of 10 healthy volunteers (age 22-39). No medication except insulin was taken for at least 10 days preceding the study. 12 h before the study all subjects received aspirin 500 mg p.o. Plasma (βTG and PF4 were determined before (basal) and 5,30,90 min after a heparin bolus i.v. (5000 U). Protein C, factor VIIIR:Ag and tissue plasminogen activator were also measured in plasma.