RELATIONSHIP BETWEEN CIRCULATING VASCULAR CELL-ADHESION MOLECULE-1 AND MICROVASCULAR COMPLICATIONS IN TYPE-2 DIABETES-MELLITUS

Citation
M. Koga et al., RELATIONSHIP BETWEEN CIRCULATING VASCULAR CELL-ADHESION MOLECULE-1 AND MICROVASCULAR COMPLICATIONS IN TYPE-2 DIABETES-MELLITUS, Diabetic medicine, 15(8), 1998, pp. 661-667
Citations number
32
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
07423071
Volume
15
Issue
8
Year of publication
1998
Pages
661 - 667
Database
ISI
SICI code
0742-3071(1998)15:8<661:RBCVCM>2.0.ZU;2-S
Abstract
The soluble form of the vascular cell adhesion molecule-1 (VCAM-1) is detectable in human sera and is elevated in diabetic patients, with un known clinical significance. In the present study, the relationship be tween serum soluble VCAM-1 and diabetic microvascular complications (r etinopathy, nephropathy, and neuropathy) was evaluated in 95 Japanese patients with Type 2 diabetes mellitus (DM). Serum soluble VCAM-1 conc entration was higher in patients with more advanced stages of retinopa thy as well as nephropathy. There was a significant correlation betwee n soluble VCAM-1 and log,, (urinary albumin excretion) in 69 patients with normal serum creatinine levels (r = 0.51, p<0.0001) and a signifi cant correlation between soluble VCAM-1 and log,, (serum creatinine) i n all the patients (r = 0.83, p<0.0001). Soluble VCAM-1 concentration was also elevated in patients with neuropathy. There was a significant correlation between soluble VCAM-1 concentration and the number of mi crovascular complications (r = 0.59, p<0.0001). However, multivariate regression analysis revealed that only diabetic nephropathy, was assoc iated with the soluble VCAM-1 concentration. The elevation of circulat ing VCAM-1 level in diabetic nephropathy may result from underlying sy stemic endothelial dysfunction, increased VCAM-1 production in damaged renal tubular or glomerular epithelial cells and/or decreased renal c learance of this molecule, depending on the stage of nephropathy. (C) 1998 John Wiley & Sons, Ltd.