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人体镁缺乏时血清1,25 - 二羟维生素D浓度降低。

Low serum concentrations of 1,25-dihydroxyvitamin D in human magnesium deficiency.

作者信息

Rude R K, Adams J S, Ryzen E, Endres D B, Niimi H, Horst R L, Haddad J G, Singer F R

出版信息

J Clin Endocrinol Metab. 1985 Nov;61(5):933-40. doi: 10.1210/jcem-61-5-933.

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-(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.

摘要

通过测量23例低钙血症性镁缺乏患者在胃肠外镁治疗前、治疗期间及治疗后5 - 13天的血清25 - 羟基维生素D(25OHD)和1,25 - 二羟基维生素D [1,25 - (OH)₂D]浓度,评估镁缺乏对维生素D代谢的影响。镁治疗使平均基础血清镁水平[1.0±0.1(均值±标准误)mg/dl]和钙水平(7.2±0.2 mg/dl)升至正常范围(分别为2.2±0.1和9.3±0.1 mg/dl;P<0.001)。给药前血清25OHD平均浓度处于正常低限范围(13.2±1.5 ng/ml),治疗后无显著变化(14.8±1.5 ng/ml)。23例患者中有16例血清1,25 - (OH)₂D水平较低(<30 pg/ml)。镁治疗后,尽管血清免疫反应性甲状旁腺激素(PTH)水平升高,但只有5例患者血清1,25 - (OH)₂D浓度升至或高于正常范围。另外1例血钙正常的低镁血症患者1,25 - (OH)₂D水平较低,镁治疗5天后未升高。对11例患者评估的血清维生素D结合蛋白浓度在镁治疗前较低(273±86 μg/ml),镁补充后恢复正常(346±86 μg/ml)。未发现与血清1,25 - (OH)₂D水平相关。在血清存在的情况下,通过肠上皮细胞内化[³H]1,25 - (OH)₂D₃评估的维生素D结合蛋白结合激素的功能能力与正常情况无显著差异(分别为11.42±1.45和10.27±1.27 fmol/2×10⁶细胞)。这些数据表明,镁缺乏患者血清1,25 - (OH)₂D浓度常常较低,即使胃肠外给予镁5 - 13天后仍可能维持在低水平。数据还提示,PTH介导的对镁给药的血钙反应不需要正常的1,25 - (OH)₂D水平。我们得出结论,镁缺乏可能损害维生素D代谢。

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