Serum magnesium level in the salt-losing type of congenital adrenal hyperplasia.

Evidence has accumulated that aldosterone plays an important part in the regulation of magnesium metabolism in experimental animals. There is, however, little information concerning the effect of aldosterone on the metabolism of magnesium in man. Mader and Iseri (1955) and Milne, Muehrcke, and Aird (1957) reported a single case of primary aldosteronism, with tetany and paralysis, in which low serum levels of magnesium and potassium were observed. Harrop et al. (1933) and Zwemer and Sullivan (1934) described high serum levels of magnesium in animals with adrenal insufficiency. Investigations have been made into the effects of mineralocorticoids upon the metabolism of magnesium and other electrolytes using adrenalectomized animals (Conway and Hingerty, 1946; Hingerty, 1957; DaVanzo, Crossfield, and Swingle, 1958; Weil and State, 1958). It has been generally agreed that serum potassium and magnesium are conspicuously raised, with parallelism in mineralocorticoid deficiency, and that mineralocorticoids increase the renal excretion of magnesium as well as of potassium. In the salt-losing type of congenital adrenal hyperplasia (CAH) which is commonly characterized by the defect of 21-hydroxylation in the biosynthesis of cortisol and aldosterone in the adrenal cortex, it is assumed that serum potassium and magnesium levels are raised. However, there have been no reports on magnesium metabolism in CAH. Accordingly, this investigation reports the serum magnesium level and its relation to other electrolytes in two infants with the salt-losing type of CAH, who were treated with mineraloand glucocorticoids plus salt supplement.