R. Kawamori et al., PLATELET ACTIVATION IN DIABETIC-PATIENTS WITH ASYMPTOMATIC ATHEROSCLEROSIS, Diabetes research and clinical practice, 24(2), 1994, pp. 89-95
We studied 27 non-insulin-dependent diabetics without apparent atheros
clerosis (AS) to investigate whether abnormal platelet function is rel
ated to asymptomatic atherosclerosis in diabetes mellitus. The degree
of AS was quantitatively evaluated by determining the intimal plus med
ial thickness (IMT) of the carotid artery wall with ultrasound high-re
solution B-mode imaging. Based on our previous finding that the upper
threshold of the IMT was 1.1 mm in healthy subjects, the patients were
divided into the AS-positive group with the IMT > 1.1 mm, (n = 17) an
d the AS-negative group with the IMT < 1.1 mm (n = 10). Among five var
iables measured as the factors concerned with thrombogenesis, only pla
sma levels of beta-thromboglobulin (beta-TG) and platelet factor 4 (PF
4) were significantly higher in the AS-positive group than in the AS-n
egative group. Chronic administration of pentoxifylline (300 mg/day) s
ignificantly reduced the abnormally high plasma levels of beta-TG and
PF4 in 7 patients of the AS-positive group to normal levels, without l
owering the normal plasma beta-TG and PF4 levels in the remaining 10 p
atients. Pentoxifylline treatment did not affect the plasma levels of
the 3 other variables, von Willebrand factor, 6-keto prostaglandin F1
alpha and thromboxane B2. This study suggests that the progress of ath
erosclerosis in diabetes mellitus is associated with in vivo platelet
activation and platelet activation does not occur in diabetics without
carotid atherosclerosis. Pentoxifylline may impede the vicious cycle
in which atherosclerosis is accelerated by platelet activation.