| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Journal of Clinical Endocrinology & Metabolism, Vol 61, 933-940, Copyright © 1985 by Endocrine Society
ARTICLES |
RK Rude, JS Adams, E Ryzen, DB Endres, H Niimi, RL Horst, JG Haddad Jr and FR Singer
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-(OH)2D] 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 less than 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 (less than 30 pg/ml). After magnesium therapy, only 5 of the patients had a rise in the serum 1,25-(OH)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 micrograms/ml) before magnesium therapy, but normalized (346 +/- 86 micrograms/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 vs. 10.27 +/- 1.27 fmol/2 X 10(6) 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.
This article has been cited by other articles:
![]() |
T. O. Carpenter, M. C. DeLucia, J. H. Zhang, G. Bejnerowicz, L. Tartamella, J. Dziura, K. F. Petersen, D. Befroy, and D. Cohen A Randomized Controlled Study of Effects of Dietary Magnesium Oxide Supplementation on Bone Mineral Content in Healthy Girls J. Clin. Endocrinol. Metab., December 1, 2006; 91(12): 4866 - 4872. [Abstract] [Full Text] [PDF] |
||||
![]() |
Z. S. AGUS Hypomagnesemia J. Am. Soc. Nephrol., July 1, 1999; 10(7): 1616 - 1622. [Full Text] |
||||
![]() |
M. Bardicef, O. Bardicef, Y. Sorokin, B. M. Altura, B. T. Altura, and L. M. Resnick Perinatal Cellular Ion Metabolism: 31P-Nuclear Magnetic Resonance Spectroscopic Analysis of Intracellular Free Magnesium and pH in Maternal and Cord Blood Erythrocytes Reproductive Sciences, March 1, 1996; 3(2): 66 - 70. [Abstract] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |