Clinical Information

Magnesium, along with potassium, is a major intracellular cation. Magnesium is a cofactor of many enzyme systems. All adenosine triphosphate (ATP)-dependent enzymatic reactions require magnesium as a cofactor. Approximately 70% of magnesium ions are stored in bone. The remainder is involved in intermediary metabolic processes; about 70% is present in free form while the other 30% is bound to proteins (especially albumin), citrates, phosphate, and other complex formers. The serum magnesium level is kept constant within very narrow limits. Regulation takes place mainly via the kidneys, primarily via the ascending loop of Henle.

Conditions that interfere with glomerular filtration result in retention of magnesium and, hence, elevation of serum concentrations. Hypermagnesemia is found in acute and chronic renal failure, magnesium overload, and magnesium release from the intracellular space. Mild-to-moderate hypermagnesemia may prolong atrioventricular conduction time. Magnesium toxicity may result in central nervous system (CNS) depression, cardiac arrest, and respiratory arrest.

Numerous studies have shown a correlation between magnesium deficiency and changes in calcium, potassium, and phosphate homeostasis, which are associated with cardiac disorders such as ventricular arrhythmias that cannot be treated by conventional therapy, increased sensitivity to digoxin, coronary artery spasms, and sudden death. Additional concurrent symptoms include neuromuscular and neuropsychiatric disorders. Conditions that have been associated with hypomagnesemia include chronic alcoholism, childhood malnutrition, lactation, malabsorption, acute pancreatitis, hypothyroidism, chronic glomerulonephritis, aldosteronism, and prolonged intravenous feeding.