The prefix hypo- means low (contrast with hyper-, meaning high). The middle magnes refers to magnesium. The end portion of the word, -emia, means 'in the blood' (note, however, that hypomagnesemia is usually indicative of a systemic magnesium deficit).
Thus, Hypomagnesemia is an electrolyte disturbance in which there is an abnormally low level of magnesium in the blood. Usually a serum level less than 0.7 mmol/l is used as reference. It must be noted that hypomagnesemia is not equal to magnesium deficiency. Hypomagnesemia can be present without magnesium deficiency and vice versa.
The body contains 21-28 grams of magnesium (1 mmol=2mEq=24.6 mg). Of this, 53% is located in bone, 19% in non-muscular tissue, and 1% in extracellular fluid. For this reason, blood levels of magnesium are not an adequate means of establishing the total amount of available magnesium.
Most of the serum magnesium is bound to chelators, (i.e. ATP, ADP, proteins and citrate). Roughly 33% is bound to proteins, and 5-10% is not bound. This "free" magnesium is essential in regulating intracellular magnesium. Normal plasma Mg is 1.7-2.3 mg/dl (0.69-0.94 mmol/l). Of this 60% is free, 33% is bound to proteins, and less than 7% is bound to citrate, bicarbonate and phosphate.
Magnesium is abundant in nature. It can be found in green vegetables, chlorophyll, coca-derivatives, nuts, wheat, seafood, and meat. It is resorbed through the small intestine, and to a lesser degree in the colon. The rectum and sigmoid colon can absorb magnesium. Hypermagnesemia has been reported after enemas containing magnesium. Forty percent of dietary magnesium is absorbed. Hypomagnesemia stimulates and hypermagnesemia inhibits this absorption.
The kidneys regulate the serum magnesium. About 2400 mg of magnesium passes through the kidneys, of which 5% (120 mg) is excreted through urine. The loop of Henle is the major site for Mg-homeostasis and 60% is resorbed.
Magnesium homeostasis comprises three systems: kidney, small intestine, and bone. In the acute phase of magnesium deficiency there is an increase in absorption in the distal small intestine and tubular resorption in the kidneys. When this condition persists serum magnesium drops and is corrected with magnesium from bone tissue. The level of intracellular magnesium is controlled through the reservoir in bone tissue.
Magnesium is a cofactor in more than 300 enzyme regulated reactions. Most importantly forming and using ATP, i.e. kinase. There is a direct effect on sodium- (Na), potassium- (K) and calcium (Ca)channels. It has several effects:
Potassium channels are inhibited by magnesium. Hypomagnesemia results in increased efflux of intracellular Mg. The cell loses potassium which then is excreted by the kidneys, resulting in hypokalemia.
Release of calcium from the sarcoplasmic reticulum is inhibited by magnesium. Low levels of magnesium stimulate the release of calcium and thereby an intracellular level of calcium. This effect similar to calcium inhibitors makes it "nature's calcium inhibitor." Lack of magnesium inhibits the release of parathyroid hormone, which can result in hypoparathyroidism and hypocalcemia. Furthermore, it makes skeletal and muscle receptors less sensitive to parathyroid hormone.
blocking N-methyl-D-aspartate, an excitatory neurotransmitter of the central nervous system.
Magnesium deficiency is not uncommon in hospitalized patients. Elevated levels of magnesium (hypermagnesemia), however, are nearly always iatrogenic. 10-20% of all hospital patients, and 60-65% of patient in the intensive care unit (ICU) have hypomagnesemia. Hypomagnesiemia is underdiagnosed, as testing for serum magnesium levels is not routine. Hypomagnesemia results in increased mortality.
Low levels of magnesium in your blood may mean either 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:
alcoholism. Hypomagnesemia occurs in 30% of alcohol abuse and 85% in delirium tremens, due to malnutrition and chronic diarrhoea. Alcohol stimulates renal excretion of magnesium, which is also increased because of alcoholic ketoacidosis, hypophosphatemia and hyperaldosteronism resulting from liver disease. Also hypomagnesemia is related to thiamine deficiency because magnesium is needed for transforming thiamine into thiamine pyrophosphate.
diuretic use (the most common cause of hypomagnesemia)
gastrointestinal causes: the distal tractus digestivus secretes high levels of magnesium. Therefore, secretory diarrhoea can cause hypomagnesemia. Thus, Crohn's disease, ulcerative colitis, Whipple's disease and coeliac sprue can all cause hypomagnesemia.
renal magnesium loss in Bartter's syndrome, postobstructive diuresis, diuretic phase of acute tubular necrosis (ATN) and kidney transplant
diabetes mellitus: 38% of diabetic outpatient clinic visits involve hypomagnesemia, probably through renal loss because of glycosuria or ketoaciduria.
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.
The diagnosis can be made by finding a plasma magnesium concentration of less than 0.7mmol/l. Since most magnesium is intracellular, a body deficit can be present with a normal plasma concentration.
In addition to hypomagnesemia, up to 40% cases will also have hypocalcemia while in up to 60% of cases, hypokalemia will also be present.
The ECG shows a prolonged QT interval.
Treatment of hypomagnesemia depends on the degree of deficiency and the clinical effects. Oral replacement is appropriate for patients with mild symptoms, while intravenous replacement is indicated for patients with severe clinical effects. Intravenous magnesium sulphate (MgSO4) can be given in the following conditions:
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Magnesium is needed for the adequate function of the Na+/K+-ATPase pumps in the cells of the heart. A lack of it depolarises and results in tachyarrhythmia. Magnesium inhibits release of potassium, a lack of magnesium increases loss of potassium. Intracellular levels of potassium decrease and the cells depolarise. Digoxin increases this effect. Both digoxin and hypomagnesemia inhibit the Na-K-pump resulting in decreased intracellular potassium.
The effect is based upon decreased excitability by depolarisation and the slowing down of electric signals in the AV-node. Magnesium is a negative inotrope as a result of decrease calcium influx and calcium release from intracellular storage. It is just as effective as verapamil. In myocardial infarction there is a functional lack of magnesium, suppletion will decrease mortality.
Convulsions are the result of cerebral vasospasm. The vasodilatatory effect of magnesium seems to be the major mechanism.
Hypokalemia: 42% of patients with hypokalemia also have hypomagnesemia, not responding to potassium supplementation. Magnesium is needed for the ATPase, Na-K-pump.
Hypocalcemia is present in 33% of patients in the intensive care unit, not responding to calcium supplementation. This is because of decreased function of the calcium pump, but also because of a decreased release of calcium by inhibition of parathyroid hormone release.
Acute asthma, here there is a bronchodilatatory effect, probably by antagonizing a calcium-mediated constriction. Also, adrenergic stimulation, i.e. sympatheticomimetics used for treatment of asthma, might lower serum levels of magnesium, which must therefore be supplemented.
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Selenium deficiency as a cause of overload of iron and unbalanced distribution of other minerals