Hypoparathyroidism During Magnesium Deficiency or Excess

Abstract

In humans, body magnesium content amounts to 25 g, with 66 % located in the bone, 33 % within cells, and only 1 % in the extracellular fluid (ECF), including blood [1–5] (see also Chap. 7). In the bone, magnesium as the divalent cation is adsorbed on the hydroxyapatite crystal and is in equilibrium with magnesium in the ECF. It is the most abundant intracellular cation together with potassium, reaching a concentration of approximately 0.5 mmol/l, which is thus close to that of magnesium in the ECF. Free cytosolic magnesium accounts for 5–10 % of total cellular magnesium. It binds to various organelles, 60 % of which is within mitochondria, where it is involved in phosphate transport, ATP synthesis, and utilization. ATP is synthesized by a magnesium-dependent oxidative phosphorylation process. Magnesium is a cofactor and regulator of a large series of enzymatic reactions, particularly those utilizing magnesium-ATP (glycolysis, oxidative phosphorylation), but also of DNA transcription and protein synthesis [1, 6]. In serum, 30 % of magnesium is protein bound. Circulating magnesium, which is between 0.7 and 1.0 mmol/l, is determined by bidirectional fluxes taking place at the levels of the intestine, kidney, and bone. Ionic magnesium interacts with the calcium-sensing receptor (CaSR) on parathyroid cells, and also on renal tubular cells, with a potency lower than calcium [7].