Low Serum Concentrations of 1,25-Dihydroxyvitamin D in Human Magnesium Deficiency

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Abstract
The effect of magnesium deficiency on vitamin D metabolism was assessed in 23 hypocalcemic magnesium-deficient patients by measuring the serum concentrations of 25-hydroxyvitamin D (25OHD) and 1,25-dihydroxyvitamin D [1,25-(OH2D] before, during, and after 5-13 days of parenteral magnesium therapy. Magnesium therapy raised mean basal serum magnesium [1.0 ± 0.1 (mean ± SEM) mg/dl] and calcium levels (7.2 ± 0.2 mg/dl) into the normal range (2.2 ± 0.1 and 9.3 ± 0.1 mg/dl, respectively; P < 0.001). The mean serum 25OHD concentration was in the low normal range (13.2 ± 1.5 ng/ml) before magnesium administration and did not significantly change after this therapy (14.8 ± 1.5 ng/ml). Sixteen of the 23 patients had low serum 1,25-(OH)2D levels (2D concentration into or above the normal range despite elevated levels of serum immunoreactive PTH. An additional normocalcemic hypomagnesemic patient (had low 1,25-(OH)2D)levels which did not rise after 5 days of magnesium therapy. The serum vitamin D-binding protein concentration, assessed in 11 patients, was low (273 ± 86 µ/ml) before magnesium therapy, but normalized (346 ± 86 Mg/ml) after magnesium repletion. No correlation with serum (1,25-(OH)2D levels was)found. The functional capacity of vitamin D-binding protein to bind hormone, assessed by the internalization of [3H]1,25-(OH)2D3 by intestinal epithelial cells in the presence of serum was not significantly different from normal (11.42 ± 1.45 us. 10.27 ± 1.27 fmol/2 × 106 cells, respectively). These data show that serum (1,25-(OH)2D concentrations are frequently low in patients with magnesium deficiency and may remain low even after 5-13 days of parenteral magnesium administration. The data also suggest that a normal 1,25-(OH)2D level is not required for the PTH-mediated calcemic response to magnesium administration. We conclude that magnesium depletion may impair vitamin D metabolism.