POLYMORPHISMS OF PLATELET GLYCOPROTEINS IN RELATION TO MACROVASCULAR DISEASE IN TYPE-2 DIABETES-MELLITUS

Citation
Am. Carter et al., POLYMORPHISMS OF PLATELET GLYCOPROTEINS IN RELATION TO MACROVASCULAR DISEASE IN TYPE-2 DIABETES-MELLITUS, Diabetic medicine, 15(4), 1998, pp. 315-319
Citations number
28
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
07423071
Volume
15
Issue
4
Year of publication
1998
Pages
315 - 319
Database
ISI
SICI code
0742-3071(1998)15:4<315:POPGIR>2.0.ZU;2-K
Abstract
We set out to determine the genotype distributions of the PIA polymorp hism of platelet glycoprotein IIIa, the HPA-3 polymorphism of platelet glycoprotein IIb, and the variable number tandem repeat (VNTR) polymo rphism of platelet glycoprotein Ib in subjects with Type 2 diabetes me llitus (Type 2 DM) with (n = 125) and without (n = 90) a clinical hist ory of macrovascular disease. In 215 white European subjects with Type 2 DM, presence of coronary artery disease was determined as a clinica l history of angina, myocardial infarction (MI), coronary angioplasty or coronary artery by-pass grafting. Presence of peripheral vascular d isease was defined as a clinical history of intermittent claudication with confirmatory vascular ultrasound or angiography, intermittent cla udication with undetectable foot pulses and no history of arthralgia o r surgery for leg ischaemia, confirmed by reference to medical case no tes. Polymorphisms were detected by polymerase chain reaction amplific ation of DNA. There was no difference in the genotype distributions of subjects with and without macrovascular disease. In subjects with a f irst MI before the age of 60 years (n = 26), there was a 38 % incidenc e of PIA2 compared to 29 % in subjects free from clinically evident ma crovascular disease, but this difference did not reach statistical sig nificance. This study does not support the hypothesis that polymorphis ms of platelet glycoproteins, in particular the PIA polymorphism of pl atelet glycoprotein IIIa, play an important role in the pathogenesis o f macrovascular disease in subjects with Type 2 DM. (C) 1998 John Wile y & Sons, Ltd.