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Does Vitamin D Modulate Asymmetric Dimethylarginine and C-Reactive Protein Concentrations?
Ist Teil von
The American journal of medicine, 2010-04, Vol.123 (4), p.335-341
Ort / Verlag
New York, NY: Elsevier Inc
Erscheinungsjahr
2010
Quelle
MEDLINE
Beschreibungen/Notizen
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.