Increased platelet Fc receptor expression in diabetes is limited to those with type 2 disease and low LDL cholesterol levels.

Abstract:

:A potential role for the platelet Fc gammaRIIA immunoreceptor (FcR) in collagen-mediated platelet activation associated with diabetes has recently been described. This study was undertaken to prospectively determine which diabetes patient population (type 1, type 2, or both) was more likely to over express platelet FcR and to determine what clinical or laboratory features characterized this population. One hundred and twenty type 2 diabetes, 135 type 1 diabetes, and 275 control patients participated in this cross-sectional study. Relative FcR expression was assessed by flow cytometry of antibody-labeled platelets. FcR expression was higher in type 2 diabetes than in type 1 diabetes or control subjects [mean+/-S.D.=15.17+/-4.66 versus 10.28+/-3.11 (p<0.05) and versus 10.33+/-2.59 (p<0.05), respectively]. This relationship was independent of sex, BMI, HDL cholesterol, triglycerides, blood pressure, glucose control, fibrinogen, and smoking. An inverse association between platelet FcR expression and plasma LDL cholesterol levels was also observed along with a modest correlation with age. Among type 2 patients there was inverse and no correlation between FcR expression and LDL levels and age respectively. Increased platelet FcR expression in type 2 diabetes may play a role in arterial vasoocclusive complications associated with this population. It is hypothesized decreased FcR expression could potentially represent a form of compensatory biological response to an adverse lipid profile in which sensitivity of platelets to collagen may be relatively down regulated in type 2 diabetes.

journal_name

Atherosclerosis

journal_title

Atherosclerosis

authors

Calverley DC,Baldermann LV,Heldt ML,Kinney GL,Hokanson JE

doi

10.1016/j.atherosclerosis.2005.06.002

keywords:

subject

Has Abstract

pub_date

2006-03-01 00:00:00

pages

173-6

issue

1

eissn

0021-9150

issn

1879-1484

pii

S0021-9150(05)00368-0

journal_volume

185

pub_type

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