In order to clarify the etiology of diabetic microangiopathy specificially in reference to platelet activity, the intra-platelet substances, β-thromboglobulin (β-TG) and platelet factor-4 (PF-4) were studied in 48 male diabetic patients.
Diabetic patients and non-diabetic control subjects were divided among the following four groups according to their degree of retinopathy: Group A, 16 control subjects; group B, 33 diabetic patients without or with on background retinopathy; group C, 7 diabetic patients with preproliferative or proliferative retinopathy without progress, and group D, 8 diabetic patients with preproliferative or proliferative retinopathy with progress.
Plasma concentration and intraplatelet contents of β-TG and PF-4, and increment of plasma PF-4 after i. v. heparin of group B were identical to those of control group A. There was a significant difference between group A and C in plasma β-TG (29.0±13.0 ng/m
l vs 51.4±25.9 ng/m
l, p<0.05) and in plasma PF-4 (8.5±4.8 ng/m
l vs 21.1±11. 2 ng/m
l, p<0.01), but no difference was found in plasma PF-4 concentration after i. v. heparin.
In group D, plasma β-TG (21.0±5.3 ng/m
l) and plasma PF-4 (4.5±1.9 ng/m
l) were low. Intraplatelet β-TG (29.8±4.6 pg/platelet) and intraplatelet PF-4 (11.2±0.9 pg/platelet) were depleted. A type of acquired storage pool deficiency is postulated primarily in group D and to a lesser extent in group C.
Although plasma β-TG and PF-4 were low in group D, the increment of plasma PF-4 after i. v. heparin was the highest. This suggests involvement of endothelial cells releasing PF-4. Platelet activity is considered to be different depending upon progressive or non-progressive retinopathy, as well as the activity of endothelial cells.
View full abstract