Table 1.

Magnesium functions and hypomagnesemia related clinical manifestations

General functions	Specific involvement	Signs/symptoms and altered metabolisms associated with hypomagnesemia*
Enzymatic activities: functioning as substrate or direct enzyme activation	Kinases, ATPases or GTPases, cyclases, phosphofructokinase, creatine kinase, 5-phosphoribosyl-pyrophosphate synthetase, adenylate cyclase, Na+-K+-ATPase	Altered glucose metabolism, electrolyte imbalances (hypokalemia, hypocalcemia), osteoporosis, enhanced digoxin sensitivity, enhanced apoptosis, arrhythmias, atherosclerosis
Membrane function	Cell adhesion, transmembrane electrolyte flux	Arrhythmias: atrial tachycardia and fibrillation, supraventricular and ventricular arrhythmias, Torsade de pointes, rhabdomyolysis, hemolysis, myocardial infarction
Calcium antagonist	Neuromuscular function	Neuromuscular hyperexcitability: tremors, fasciculation, tetany, convulsions, neuropsychiatric changes, eg, apathy, depression, psychosis, vertigo, nystagmus, athetoid movements and choreiform movements, migraine, asthma (reactive airways), impaired exercise performance, electrolyte imbalances (hypokalemia, hypocalcemia), hypertension, atherosclerosis
Structural function, ion complex formation	Proteins, polyribosomes, nucleic acids, multiple enzyme complexes, mitochondria, ion complexes	Enhanced apoptosis, osteoporosis, kidney stones

Notes: Copyright © 2003. Australasian Association of Clinical Biochemists. Adapted from Swaminathan R. Magnesium metabolism and its disorders. Clin Biochem Rev. 2003;24(2):47–66.3

^*Signs and symptoms are listed based on possible and/or presumed mechanisms of hypomagnesemia-induced defective structural or physiological functions. Many signs and symptoms are multifactorial, not fully understood, and beyond the scope of the current paper.

Abbreviations: ATPase, adenosine triphosphatase; GTPase, guanosine triphosphatase; Na⁺-K⁺-ATPase, sodium-potassium adenosine triphosphatase.