Does Vitamin D modulate asymmetric dimethylarginine and C-reactive protein concentrations?
Date
2010
Authors
Ngo, D.
Sverdlov, A.
McNeil, J.
Horowitz, J.
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Journal article
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American Journal of Medicine, 2010; 123(4):335-341
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Doan T. Ngo, Aaron L. Sverdlov, John J. McNeil, and John D. Horowitz
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Abstract
Background: Vitamin D deficiency is associated with significant increases in the incidence of cardiovascular risk factors and mortality. However, the mechanisms underlying this association remain unclear. The current study evaluated the possible relationships among vitamin D status, endothelial dysfunction, and inflammation. Methods: Plasma concentrations of 25-hydroxyvitamin D3 were determined by radioimmunoassay in a normal population cohort (n = 253) aged 51 to 77 years (mean 63.4 ± 6 years). Asymmetric dimethylarginine, a marker/mediator of endothelial dysfunction, was assayed by high-performance liquid chromatography. High-sensitivity C-reactive protein levels were used as a marker of inflammatory activation. Results: On univariate analyses, low 25-hydroxyvitamin D3 levels were inversely correlated with asymmetric dimethylarginine concentrations, high-sensitivity C-reactive protein levels, and body mass index. Seasonal fluctuations in 25-hydroxyvitamin D3 levels were associated with reciprocal asymmetric dimethylarginine concentration fluctuations. Hypertension and treatment with an angiotensin-converting enzyme inhibitor/angiotensin receptor blocker also were associated with low 25-hydroxyvitamin D3 levels. On multiple linear analysis, both asymmetric dimethylarginine (β = −0.19, P = .003) and high-sensitivity C-reactive protein (β = −0.14, P = .03) concentrations were inversely correlated with plasma 25-hydroxyvitamin D3 concentrations; other significant correlates were male gender (β = 0.19, P = .003), calcium levels (β = 0.14, P = .03), and use of angiotensin-converting enzyme inhibitor (β = −0.17, P = .007). Conclusion: Low 25-hydroxyvitamin D3 levels are associated with markers of endothelial dysfunction and inflammatory activation, representing potential mechanisms for incremental coronary risk.
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© 2010 Elsevier Inc. All rights reserved.