4.4 Article

Circulating monocytes in patients with diabetes mellitus, arterial disease, and increased CD14 expression

Journal

AMERICAN JOURNAL OF CARDIOLOGY
Volume 85, Issue 11, Pages 1288-1291

Publisher

EXCERPTA MEDICA INC
DOI: 10.1016/S0002-9149(00)00757-8

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Low serum concentrations of high-density lipoprotein (HDL) cholesterol and elevated levels of acute-phase reactans are frequently found in patients with non-insulin-dependent diabetes mellitus (NIDDM) and cardiovascular disease. Changes in the phenotype of circulating monocytes have been reported with both of these circumstances in nondiabetic subjects. In the present study, we explored the possibility that similar changes may occur in circulating monocytes of patients with NIDDM and arterial disease. Two groups of subjects with NIDDM were studied: patients with cardiovascular disease (n = 25) were compared with a group without cardiovascular disease (n = 26); both groups were age- and sex-matched, had the same length of diabetes duration, and degree of glycemic control. Healthy nondiabetic volunteers of comparable age and sex (n = 35) formed the control group. There was no significant difference in the numbers of the CD14+/CD16+ monocyte subpopulations between the 3 groups. However, a significant graded increase of the mCD14 intensity expression values was observed among the groups, with the highest levels in patients with NIDDM patients and the lowest in nondiabetic subjects. The serum C-reactive protein concentrations were significantly higher in the group with arterial disease compared with those without arterial disease or healthy controls. in the group of patients as a whole, relative mCD14 intensity expression was significantly correlated with HDL cholesterol levels (inversely) and with serum concentrations of C-reactive protein. Serum HDL cholesterol levels and the C-reactive protein concentrations were also significantly for related. We concluded that the increased mCD14 intensity expression on circulating monocytes may be an important contributor to the increased inflammatory response observed in patients with NIDDM and arterial disease, and eventually, to atherogenesis. (C) 2000 by Excerpta Medico, Inc.

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