Magnesium deficiency is an electrolyte disturbance in which there is a low level of magnesium in the body. Symptoms include tremor, poor coordination, muscle spasms, loss of appetite, personality changes, and nystagmus. Complications may include seizures or cardiac arrest such as from torsade de pointes. Those with low magnesium often have low potassium. Causes include low dietary intake, alcoholism, diarrhea, increased urinary loss, and poor absorption from the intestines. Some medications may also cause low magnesium, including proton pump inhibitors (PPIs) and furosemide. The diagnosis is typically based on finding low blood magnesium levels, also called hypomagnesemia. Normal magnesium levels are between 0.6 and 1.1 mmol/L (1.46–2.68 mg/dL) with levels less than 0.6 mmol/L (1.46 mg/dL) defining hypomagnesemia. Specific electrocardiogram (ECG) changes may be seen. Treatment is with magnesium either by mouth or intravenously. For those with severe symptoms, intravenous magnesium sulfate may be used. Associated low potassium or low calcium should also be treated. The condition is relatively common among people in hospitals.
Signs and symptoms Deficiency of magnesium can cause tiredness, generalized weakness, muscle cramps, abnormal heart rhythms, increased irritability of the nervous system with tremors, paresthesias, palpitations, low potassium levels in the blood, hypoparathyroidism which might result in low calcium levels in the blood, chondrocalcinosis, spasticity and tetany, migraines, epileptic seizures, basal ganglia calcifications and in extreme and prolonged cases coma, intellectual disability or death. Magnesium deficiency is strongly associated with and appears to contribute to obesity, insulin resistance, metabolic syndrome, and type 2 diabetes, although the causal mechanism is not fully understood.
Causes Magnesium deficiency may result from gastrointestinal or kidney causes. Gastrointestinal causes include low dietary magnesium intake, reduced gastrointestinal absorption, or increased gastrointestinal loss due to rapid gastrointestinal transits. Kidney causes involve increased excretion of magnesium. Poor dietary intake of magnesium has become an increasingly important factor: many people consume diets high in refined foods such as white bread and polished rice, which have been stripped of magnesium-rich plant fiber. Magnesium deficiency is common in hospitalized patients. Up to 12% of all people admitted to hospital, and as high as 60–65% of people in an intensive care unit (ICU), have hypomagnesemia. About 57% of the US population does not meet the US RDA for dietary magnesium intake. Kidneys are very efficient at maintaining body levels; however, if the diet is deficient, or certain medications such as diuretics or proton pump inhibitors are used, or in chronic alcoholism, levels may drop. Deficiencies may be due to the following conditions:
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, high dosage 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 increasing 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.
Genetics 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, especially mutations in the mitochondrial tRNAs MT-TI or MT-TF. Mutations in SARS2, or mitochondrial DNA deletions as seen with Kearns-Sayre syndrome, can also cause hypomagnesemia, 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 or sunlight exposure, or vitamin B6, Gastrointestinal causes: the distal digestive tract 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,
Other Chronic alcoholism: Alcohol intake leads to enhanced diuresis of electrolytes, possibly due to alcohol-induced kidney tubular cell damage. Hypomagnesemia is also thought to occur due to reduced magnesium intake due to malnutrition and increased gastrointestinal losses. Hypomagnesemia is the most common electrolyte abnormality in those with chronic alcoholism. Chronic hypomagnesemia in those with chronic alcoholism is associated with liver disease and a worse prognosis, 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.
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