Hypovitaminosis is believed to have wide-ranging influences on vascular physiology

Hence, the inverse associations of 25 D with tPA and D-dimer observed in our study support the role of vitamin D metabolism in maintaining antithrombotic homeostasis. The direct influences of hormonal vitamin D axis on hemostasis are not well established, although recent gene-expression studies suggest that vitamin D analogues may suppress thrombogenicity and enhance fibrinolysis thereby reducing intimal plaque formation. Vitamin D analogues have been observed to suppress PAI-1 expression in human coronary artery smooth muscle cells. Up regulation of PAI-1 has been associated with increased risk of CVD, and it has been suggested that suppression of PAI-1 expression may contribute to the observations on improved survival among patients with chronic kidney disease who are taking vitamin D analogues. Hypovitaminosis D is believed to have wide-ranging influences on vascular physiology, which include both direct and indirect pathways. Vitamin D toxicity has been associated with adverse effects on vascular calcification, but available data indicates that Lucidenic-acid-E calcification is increased also in hypovitaminosis D. Associations with increased blood pressure are believed to be mediated through decreased renin production and it has been suggested that, this could also affect vascular stiffness. Vitamin D might also exert antiproliferative effects on vascular smooth muscle cells, thereby affecting myocardial cell hypertrophy and proliferation. Discussion regarding optimal status for 25 D concentration is ongoing, and there is some debate about whether a threshold exists. The curved association between 25 D and D-dimer, together with the suggestive elevations in fibrinogen and CRP at the extreme of high concentrations observed in this study, could support a threshold effect with the optimal concentration being between 60 and 120nmol/l. These results are in line with an evaluation using data on multiple health outcomes, which corresponds to an beta-chamigrenic-acid earlier consensus statement on osteoporosis suggesting 75nmol/l as the lower reference value.

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