Platelet aggregation in type 1 diabetes without microvascular disease during continuous subcutaneous insulin infusion.

The effect of metabolic control on platelet activities was studied in eleven insulin-dependent diabetic patients during six months of continuous insulin infusion (CSII) treatment in comparison to three months of conventional therapy. Diabetic patients chosen for the study were free of microvascular disease. Glycemia control was improved during CSII treatment and a significant hemoglobin A1c reduction from 8.26 +/- 1.78 to 6.16 +/- 0.46%, p < 0.001, was achieved. The accompanying improvement in platelet aggregation in response to two agonists was only observed with the achievement of glycemia control (ADP: 20.84 +/- 4.61 vs 14.84 +/- 3.03%, p < 0.001; arachidonic acid: 22.04 +/- 4.26 vs 16.0 +/- 3.15%, p < 0.01). The synthesis of proaggregatory thromboxane B2, as a response to arachidonate, was lower during the CSII period (TxB2: 415 +/- 51 vs 382 +/- 36 micrograms/l.10(6) platelets), but with no statistical significance. Inspite of the fact that in all patients, lipoprotein concentrations were of normal values both before and after intensified therapy (HDL-c: 1.48 +/- 0.5 vs 1.52 +/- 0.4 mmol/l, NS; LDL-c: 3.2 +/- 1.3 vs 2.7 +/- 1.0 mmol/l, NS), a significant correlation was observed between the atherogenic lipoprotein fraction and aggregation parameters. Thus, in all patients, LDL-cholesterol before and during CSII showed a significant correlation with platelet sensitivity to ADP (r = 0.61, p < 0.002), whereas at the same time its correlation with the corresponding values of HDL-cholesterol (r = -0.52, p < 0.01) was negative. Our results suggested that intensive insulin treatment reduced platelet aggregation in patients without microvascular disease when strict glycemia control was maintained and indicated that changes in platelet aggregation could directly result from changes in plasma glucose concentrations.