Increased platelet malondialdehyde, but normal platelet sensitivity to adenosine-5-diphosphate and prostacyclin in well-controlled type 1 diabetics without vascular complications.

Normal platelet sensitivity to in vitro ADP-induced aggregation (median 46, range 32-62% dT) and a normal antiaggregatory effect of prostacyclin (PGI2; ID50:0.65, range 0.18-2 ng PGI2/ml PRP) were found in a carefully selected group of 30 fairly well-controlled (average HbA1c 7.0%) Type 1 diabetic patients (14m/16f; median age 27.5, range 15-45 yr; duration of disease 7, range 1-24 yr) without macroangiopathy in comparison to 19 (9m/10f; age 26, range 17-40 yr) closely matched healthy controls (42, range 34-63% dT; 0.55, range 0.35-1 ng PGI2/ml PRP). By contrast, platelet malondialdehyde (MDA) release was significantly (p less than 0.001; Mann-Whitney, two-tailed, non-parametric test) increased in diabetics (6.55, range 0.91-18.94 nmol/10(9) platelets) in comparison to controls (3.9 range 2.6-6.9 nmol/10(9) platelets). Since MDA has been used as an indicator of platelet thromboxane formation (a potent stimulator of platelet aggregation), elevated platelet MDA in diabetics has been attributed to platelet activation. In the present study, for the first time increased platelet MDA release in diabetics has been shown to occur independently from enhanced platelet aggregation, even in well-controlled patients without evidence of either macroangiopathy or microangiopathy. This could be of clinical importance, since MDA is known to act on low density lipoprotein-uptake of human macrophages.