PLATELET ACTIVATION IN DIABETIC-PATIENTS WITH ASYMPTOMATIC ATHEROSCLEROSIS

Citation
R. Kawamori et al., PLATELET ACTIVATION IN DIABETIC-PATIENTS WITH ASYMPTOMATIC ATHEROSCLEROSIS, Diabetes research and clinical practice, 24(2), 1994, pp. 89-95
Citations number
38
Categorie Soggetti
Gastroenterology & Hepatology","Endocrynology & Metabolism
ISSN journal
01688227
Volume
24
Issue
2
Year of publication
1994
Pages
89 - 95
Database
ISI
SICI code
0168-8227(1994)24:2<89:PAIDWA>2.0.ZU;2-P
Abstract
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.