Magnesium deficit in major burns: role in hypoparathyroidism and end-organ parathyroid hormone resistance.
Children and adults who are severely burned develop magnesium(Mg) depletion, hypocalcemia, hypoparathyroidism and renal resistance to the administration of exogenous parathyroid hormone(PTH). This same spectrum of findings is seen with both Mg depletion and hypermagnesemia. We reported that in a group of ten children burned at least 30 per cent of total body surface area that 70-80 per cent of serum levels of ionized calcium and Mg were low. In three of the patients studies when serum Mg returned to normal, retention of a standard Mg infusion was abnormally high in two of them, suggesting persistence of Mg depletion despite normal serum Mg levels. Mg intake in these children conforms to the recommended dietary intake for age suggesting that excessive Mg losses may contribute to the observed Mg depletion. These losses are through the burn wound and possibly through abnormal intestinal secretion. Increased metabolic rate seen in burn patients may also promote intracellular Mg uptake to support the increased energy requirements of cells. It is hypothesized that since Mg is an important cofactor in the production of cyclic AMP, Mg deficiency may block intracellular cyclic AMP generation in parathyroid cells to block the secretion of parathyroid hormone and in renal tubular cells to block the renal generation may improve PTH secretion and hypocalcemia in non-burned patients, preliminary data in burned children suggest that the cause of hypocalcemia and hypoparathyroidism is more complex.