Plasma concentration of C-reactive protein is increased in type I diabeticpatients without clinical macroangiopathy and correlates with markers of endothelial dysfunction: evidence for chronic inflammation
Cg. Schalkwijk et al., Plasma concentration of C-reactive protein is increased in type I diabeticpatients without clinical macroangiopathy and correlates with markers of endothelial dysfunction: evidence for chronic inflammation, DIABETOLOG, 42(3), 1999, pp. 351-357
Moderately increased plasma concentrations of C-reactive protein are associ
ated with an increased risk of cardiovascular disease. C-reactive protein,
its relation to a low degree of inflammatory activation and its association
with activation of the endothelium have not been systematically investigat
ed in Type I (insulin-dependent) diabetes mellitus. C-reactive protein conc
entrations were measured in 40 non-smoking patients with Type I diabetes wi
thout symptoms of macrovascular disease and in healthy control subjects, an
d in a second group of Type I diabetic patients (n = 60) with normo- (n = 2
0), micro-(n = 20) or macroalbuminuria (n = 20). Differences in glycosylati
on of alpha(1)-acid glycoprotein were assayed by crossed affinity immunoele
ctrophoresis. Activation of the endothelium was measured with plasma concen
trations of endothelial cell markers. The median plasma concentration of C-
reactive protein was higher in Type I diabetic patients compared with healt
hy control subjects [1.20 (0.06-21.64) vs 0.51 (0.04-9.44) mg/l; p < 0.02].
The Type I diabetic subjects had a significantly increased relative amount
of fucosylated alpha(1)-acid glycoprotein (79 +/- 12% vs 69 +/- 14% in the
healthy control subjects; p < 0.005), indicating a chronic hepatic inflamm
atory response. In the Type I diabetic group, log(C-reactive protein) corre
lated significantly with von Willebrand factor (r = 0.439, p < 0.005) and v
ascular cell adhesion molecule-1 (r = 0.384, p < 0.02), but not with sE-sel
ectin (r = 0.008, p = 0.96). In the second group of Type I diabetic patient
s, increased urinary albumin excretion was associated with a significant in
crease of von Willebrand factor (p < 0.0005) and C-reactive protein (p = 0.
003), which were strongly correlated (r = 0.53, p < 0.0005). Plasma concent
rations of C-reactive protein were higher in Type I diabetic patients witho
ut (clinical) macroangiopathy than in control subjects, probably due to a c
hronic hepatic inflammatory response. The correlation of C-reactive protein
with markers of endothelial dysfunction suggests a relation between activa
tion of the endothelium and chronic inflammation.