Magnesium deficiency is not uncommon in hospitalized patients. Elevated levels of magnesium (hypermagnesemia), however, are nearly always caused by a medical treatment. Up to 12 percent of all people admitted to hospital and as high as 60–65% of people in the intensive care unit (ICU) have hypomagnesemia. Hypomagnesemia is probably underdiagnosed, as testing for serum magnesium levels is not routine.
Low levels of magnesium in blood may mean that there is not enough magnesium in the diet, the intestines are not absorbing enough magnesium, or the kidneys are excreting too much magnesium. Deficiencies may be due to the following conditions:
Drugs => Alcoholism. Hypomagnesemia occurs in 30% of alcohol abusers and in 85% of delirium tremens inpatients, due to malnutrition and chronic diarrhea. Alcohol stimulates the kidneys' excretion of magnesium, which is also increased because of alcoholic and diabetic ketoacidosis, low blood phosphate levels, and hyperaldosteronism resulting from liver disease. Also, hypomagnesemia is related to thiamine deficiency because magnesium is needed for transforming thiamine into thiamine pyrophosphate.
- Medications => Loop and thiazide diuretic use (the most common cause of hypomagnesemia)
- Antibiotics (i.e. Aminoglycoside, amphotericin, pentamidine, gentamicin, tobramycin, viomycin) block resorption in the loop of Henle. 30% of patients using these antibiotics have hypomagnesemia.
- Long term use of proton-pump inhibitors such as omeprazole.
- Other drugs. Digitalis, displaces magnesium into the cell. Digitalis causes an increased intracellular concentration of sodium, which in turn increases intracellular calcium by passively decreasing the action of the sodium-calcium exchanger in the sarcolemma. The increased intracellular calcium gives a positive inotropic effect. Adrenergics, displace magnesium into the cell Cisplatin, stimulates kidney excretion Ciclosporin, stimulates kidney excretion Mycophenolate mofetil
- Digitalis, displaces magnesium into the cell. Digitalis causes an increased intracellular concentration of sodium, which in turn increases intracellular calcium by passively decreasing the action of the sodium-calcium exchanger in the sarcolemma. The increased intracellular calcium gives a positive inotropic effect.
- Adrenergics, displace magnesium into the cell
- Cisplatin, stimulates kidney excretion
- Ciclosporin, stimulates kidney excretion
- Mycophenolate mofeti.
- Genetic causes => Gitelman-like diseases, which include the syndromes caused by genetic mutations in SLC12A3, CLNCKB, BSND, KCNJ10, FXYD2, HNF1B or PCBD1. In these diseases, the hypomagnesemia is accompanied by other defects in electrolyte handling such as hypocalciuria and hypokalemia. The genes involved in this group of diseases all encode proteins that are involved in reabsorbing electrolytes (including magnesium) in the distal convoluted tubule of the kidney.
- Hypercalciuric hypomagnesemic syndromes, which encompass the syndromes caused by mutations in CLDN16, CLDN19, CASR or CLCNKB. In these diseases, reabsorption of divalent cations (such as magnesium and calcium) in the thick ascending limb of Henle's loop of the kidney is impaired. This results in loss of magnesium and calcium in the urine.
- Mitochondriopathies, such as caused by mutations in SARS2, MT-TI or as seen with Kearns-Sayre syndrome.
- Other genetic causes of hypomagnesemia, such as mutations in TRPM6, CNNM2, EGF, EGFR, KCNA1 or FAM111A. Many of the proteins encoded by these genes play a role in the transcellular absorption of magnesium in the distal convoluted tubule.
- Metabolic abnormalities => Insufficient selenium, vitamin D, sunlight exposure or vitamin B6.
- Gastrointestinal causes: the distal tractus digestivus secretes high levels of magnesium. Therefore, secretory diarrhea can cause hypomagnesemia. Thus, Crohn's disease, ulcerative colitis, Whipple's disease and celiac sprue can all cause hypomagnesemia.
- Postobstructive diuresis, diuretic phase of acute tubular necrosis (ATN) and kidney transplant. Citation needed.
- Other => Acute myocardial infarction: within the first 48 hours after a heart attack, 80% of patients have hypomagnesemia. This could be the result of an intracellular shift because of an increase in catecholamines.
- Malabsorption
- Acute pancreatitis
- Fluoride poisoning
- Massive transfusion (MT) is a lifesaving treatment of hemorrhagic shock, but can be associated with significant complications.
The diagnosis can be made by finding a plasma magnesium concentration of less than 0.6 mmol/L (1.46 mg/dl). Since most magnesium is intracellular, a body deficit can be present with a normal plasma concentration.
The ECG may show a tachycardia with a prolonged QT interval, which has been noted in proton pump inhibitor-associated hypomagnesemia.
Deficiency of magnesium can cause tiredness, generalized weakness, muscle cramps, abnormal heart rhythms, increased irritability of the nervous system with tremors, paresthesias, palpitations, hypokalemia, hypoparathyroidism which might result in hypocalcemia, chondrocalcinosis, spasticity and tetany, epileptic seizures, basal ganglia calcifications and in extreme and prolonged cases coma, intellectual disability or death. Other symptoms that have been suggested to be associated with hypomagnesemia are athetosis, jerking, nystagmus, and an extensor plantar reflex, confusion, disorientation, hallucinations, depression, hypertension and fast heart rate.
People being treated on an intensive care unit who have a low magnesium level may have a higher risk of requiring mechanical ventilation, and death.