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Impaired trace element metabolism may be involved in some of the metabolic dysfunctions, and contribute to the development of vascular complications in diabetic patients. In order to investigate the relationships among diabetes mellitus, trace element status, leukocyte activation and vascular complications, 55 type 2 diabetic patients (34 with vascular complications and 21 without vascular complications) and 50 non-diabetic control subjects were studied. The mean leukocyte count (p&lt;0.001), polymorphonuclear elastase (p&lt;0.001), erythrocyte malondialdehyde (p&lt;0.001), and glycated haemoglobin (p&lt;0.001) levels, and copper/zinc ratio (p&lt;0.001) were found to be higher in diabetic patients than in the control group, but serum zinc levels (p&lt;0.001) and erythrocyte superoxide dismutase activities (p&lt;0.001) were lower, and serum copper levels showed no differences. In patients with vascular complications, the mean leukocyte count (p&lt;0.05), zinc (p&lt;0.05), polymorphonuclear elastase (p&lt;0.05), erythrocyte malondialdehyde (p&lt;0.001) and glycated haemoglobin (p&lt;0.05) levels, and copper/zinc ratio (p&lt;0.001) were significantly different from those patients without complications. Closer correlations between the copper/zinc ratio and polymorphonuclear elastase (r=0.82, p&lt;0.01), erythrocyte malondialdehyde (r=0.46, p&lt;0.05) or erythrocyte superoxide dismutase (r= −0.85, p&lt;0.01) were found in patients with vascular complications compared to those without, and all of those showed significant relationships with poor glycaemic metabolic control. We conclude that zinc deficiency may provoke polymorphonuclear leukocyte activation, and contributes to the development of vascular complications in type 2 diabetic patients. Furthermore, copper/zinc ratio and polymorphonuclear elastase may be used as important markers to evaluate the presence of vascular complications.

clinical chemistry and laboratory medicine

The Effects of Impaired Trace Element Status on Polymorphonuclear Leukocyte Activation in the Development of Vascular Complications in Type 2 Diabetes Mellitus