ABSTRACT
The concentration of magnesium in plasma and erythrocytes fell moderately. Because the muscle magnesium content re-mained normal, the presumption was that bone was the source of the loss. Urinary and fecal magnesium decreased markedly, as did urinary calcium. At the height of the deficiency, the plasma magnesium concentration fell to a range of 10 to 30% of the control values, while the red cell magnesium declined more slowly and to a smaller degree. When magnesium was added to the experimental diet, all clinical and biochemical abnormalities were corrected. Magnesium deficiency can occur in congestive heart failure, after diuresis, with furosemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delirium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with primary hypoparathyroidism, primary aldosteronism, juxtaglomerular hyperplasia, and pancreatitis. Prolonged fasting is associated with a continued renal excretion of magnesium.
