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Plasma concentration of C-reactive protein is increased in Type I diabetic patients without clinical macroangiopathy and correlates with markers of endothelial dysfunction: Evidence for chronic inflammation

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Author: Schalkwijk, C.G. · Poland, D.C.W. · Dijk, W. van · Kok, A. · Emeis, J.J. · Dräger, A.M. · Doni, A. · Hinsbergh, V.W.M. van · Stehouwer, C.D.A.
Type:article
Date:1999
Institution: Gaubius instituut TNO
Source:Diabetologia, 3, 42, 351-357
Identifier: 234978
doi: doi:10.1007/s001250051162
Keywords: Biology · α1-Acid glycoprotein · Acute-phase response · Atherosclerosis · C- reactive protein · Fucosylation · Type I (insulin-dependent) diabetes mellitus · Vascular disease · Adult · Albuminuria · Biological Markers · Body Mass Index · C-Reactive Protein · Diabetes Mellitus, Type 1 · Diabetic Angiopathies · E-Selectin · Endothelium, Vascular · Female · Fibrinogen · Hemoglobin A, Glycosylated · Humans · Inflammation · Male · Orosomucoid · Phospholipases A · Reference Values · Regression Analysis · Vascular Cell Adhesion Molecule-1 · von Willebrand Factor

Abstract

Moderately increased plasma concentrations of C-reactive protein are associated 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 investigated in Type I (insulin-dependent) diabetes mellitus. C-reactive protein concentrations were measured in 40 non-smoking patients with Type I diabetes without symptoms of macrovascular disease and in healthy control subjects, and in a second group of Type I diabetic patients (n = 60) with normo- (n = 20), micro- (n = 20) or macroalbuminuria (n = 20). Differences in glycosylation of α1-acid glycoprotein were assayed by crossed affinity immunoelectrophoresis. Activation of the endothelium was measured with plasma concentrations of endothelial cell markers. The median plasma concentration of C-reactive protein was higher in Type I diabetic patients compared with healthy 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 α1-acid glycoprotein (79 ± 12% vs 69 ± 14% in the healthy control subjects; p < 0.005), indicating a chronic hepatic inflammatory response. In the Type I diabetic group, log(C-reactive protein) correlated significantly with von Willebrand factor (r = 0.439, p < 0.005) and vascular cell adhesion molecule-1 (r = 0.384, p < 0.02), but not with sE- selectin (r = 0.008, p = 0.96). In the second group of Type I diabetic patients, increased urinary albumin excretion was associated with a significant increase 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 concentrations of C-reactive protein were higher in Type I diabetic patients without (clinical) macroangiopathy than in control subjects, probably due to a chronic hepatic inflammatory response. The correlation of C-reactive protein with markers of endothelial dysfunction suggests a relation between activation of the endothelium and chronic inflammation.