MAGNESIUM-METABOLISM IN CHILDHOOD

Hypomagnesemia in childhood is relatively frequently noted in the neon atal period due to maternal causes, such as decreased intake due to vo miting, overuse of laxatives, and neonatal causes such as intrauterine growth retardation, birth asphyxia and exchange transfusion. A very r are cause of neonatal magnesium deficiency is called primary hypomagne semia caused by impaired intestinal absorption of magnesium. Reference values of serum magnesium in cord blood are slightly lowered. Erythro cyte magnesium content is also lowered in cord blood and during the fi rst month after birth. Mononuclear magnesium content shows no differen ces with age. Renal magnesium loss is diagnosed by the presence of hyp omagnesemia with an inappropriately high 24-hour urinary magnesium exc retion. In isolated familial hypomagnesemia an autosomal dominant as w ell as an autosomal recessive mode of inheritance was found. The renal magnesium treshold is lowered in both forms but the tubular maximum i s only lowered in the dominant form. In familial hypomagnesemia-hypoka lemia (Gitelman syndrome) the renal magnesium treshold is lowered but the tubular maximum is in the normal range. In this syndrome, with pro bably an autosomal recessive mode of inheritance, the renal defect mig ht be located in the distal nephron after the medullary part of the as cending limb of the loop of Henle. The magnesium content of mononuclea r cells and erythrocytes is in the normal and lower normal range, resp ectively. In the familial hypomagnesemia-hypercalciuria syndrome, hypo magnesemia is always combined with hyperuricemia and nephrocalcinosis. Myopia and horizontal nystagmus are often present.