Michio Otsuki
Department School of Medicine(Tokyo Women's Medical University Hospital), School of Medicine Position Professor and Division head |
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Article types | Original article |
Language | English |
Peer review | Peer reviewed |
Title | Relationship between circulating vascular cell adhesion molecule-1 and microvascular complications in type 2 diabetes mellitus |
Journal | Formal name:Diabetic medicine : a journal of the British Diabetic Association Abbreviation:Diabet Med ISSN code:07423071 (Print)07423071 (Linking) |
Domestic / Foregin | Foregin |
Volume, Issue, Page | 15(8),pp.661-667 |
Author and coauthor | Koga, M. Otsuki, M. Kubo, M. Hashimoto, J. Kasayama, S. |
Authorship | 2nd author |
Publication date | 1998 |
Summary | The soluble form of the vascular cell adhesion molecule-1 (VCAM-1) is detectable in human sera and is elevated in diabetic patients, with unknown clinical significance. In the present study, the relationship between serum soluble VCAM-1 and diabetic microvascular complications (retinopathy, nephropathy, and neuropathy) was evaluated in 95 Japanese patients with Type 2 diabetes mellitus (DM). Serum soluble VCAM-1 concentration was higher in patients with more advanced stages of retinopathy as well as nephropathy. There was a significant correlation between soluble VCAM-1 and log10 (urinary albumin excretion) in 69 patients with normal serum creatinine levels (r = 0.51, p<0.0001) and a significant correlation between soluble VCAM-1 and log10 (serum creatinine) in 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 microvascular complications (r = 0.59, p<0.0001). However, multivariate regression analysis revealed that only diabetic nephropathy, was associated with the soluble VCAM-1 concentration. The elevation of circulating VCAM-1 level in diabetic nephropathy may result from underlying systemic endothelial dysfunction, increased VCAM-1 production in damaged renal tubular or glomerular epithelial cells and/or decreased renal clearance of this molecule, depending on the stage of nephropathy. |
DOI | 10.1002/(SICI)1096-9136(199808)15:8<661::AID-DIA645>3.0.CO;2-G |
Document No. | 9702469 |