Don’t be “D”-ceived by vitamin D levels

Abstract

One would think that something as seemingly straightforward as the normal range for the serum concentration of vitamin D (25(OH)D) would be fairly well established, especially with the growing current interest in calcium and vitamin D nutrition. Unfortunately, this is not the case.In states of dietary vitamin D deficiency assessed by measuring the serum level of 25(OH)D, there is enhanced hydroxylation of the substrate, resulting in increasing concentrations of 1,25(OH)2D. Thus, when individuals who are vitamin D deficient are given oral vitamin D, their 1,25(OH)2D levels increase. In contrast, providing additional oral vitamin D to individuals who are D sufficient has no effect on their 1,25(OH)2D levels.Complicating this already complex situation is the situation of dietary calcium deficiency. Although not commonly seen in US children, this is a common cause of rickets in Nigeria. In the current issue of The Journal, Thacher et al studied 16 Nigerian children with established calcium deficient rickets. They provided a single oral does of vitamin D to these children, and then examined their vitamin D metabolites. The children experienced an increase in 1,25(OH)2D similar to that seen in vitamin D deficient individuals, suggesting that calcium deficiency increases the demand for vitamin D to maintain 1,25(OD)2D levels. This observation has interesting implications. It suggests that “normal” values for 25(OH)D may be somewhat affected by dietary calcium intake. It also reminds us that there may be an increased need for vitamin D in states of calcium deficiency rickets. One would think that something as seemingly straightforward as the normal range for the serum concentration of vitamin D (25(OH)D) would be fairly well established, especially with the growing current interest in calcium and vitamin D nutrition. Unfortunately, this is not the case. In states of dietary vitamin D deficiency assessed by measuring the serum level of 25(OH)D, there is enhanced hydroxylation of the substrate, resulting in increasing concentrations of 1,25(OH)2D. Thus, when individuals who are vitamin D deficient are given oral vitamin D, their 1,25(OH)2D levels increase. In contrast, providing additional oral vitamin D to individuals who are D sufficient has no effect on their 1,25(OH)2D levels. Complicating this already complex situation is the situation of dietary calcium deficiency. Although not commonly seen in US children, this is a common cause of rickets in Nigeria. In the current issue of The Journal, Thacher et al studied 16 Nigerian children with established calcium deficient rickets. They provided a single oral does of vitamin D to these children, and then examined their vitamin D metabolites. The children experienced an increase in 1,25(OH)2D similar to that seen in vitamin D deficient individuals, suggesting that calcium deficiency increases the demand for vitamin D to maintain 1,25(OD)2D levels. This observation has interesting implications. It suggests that “normal” values for 25(OH)D may be somewhat affected by dietary calcium intake. It also reminds us that there may be an increased need for vitamin D in states of calcium deficiency rickets. Early response to vitamin D2 in children with calcium deficiency ricketsThe Journal of PediatricsVol. 149Issue 6PreviewTo assess the effect of vitamin D2 administration on serum vitamin D metabolite concentrations in calcium deficiency rickets. Full-Text PDF