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Magnesium
ICD-10 E83.4
ICD-9 275.2
DiseasesDB 6469
MedlinePlus 000315
med/3382
eMedicine emerg/274
ped/1122
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.
It may result from a number of conditions including inadequate intake of magnesium, chronic
diarrhea, malabsorption, alcoholism, chronic stress, diuretic use and other disorders.
Contents
1 Homeostasis
2 Metabolism
3 Causes
4 Clinical Features
5 Investigations
6 Treatment
o
6.1 Arrhythmia
6.2 Obstetric
6.4 Pulmonary
7 References
8 See also
9 External links
Homeostasis
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, cocoaderivatives, 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.
Metabolism
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:
Causes
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:
other drugs
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excess calcium
excess salt
insufficient selenium
insufficient vitamin B6
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.
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
Clinical Features
Investigations
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
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:
Arrhythmia
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because it lacks in-text citations.
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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.
Magnesium intravenously helps in refractory arrhythmia, most notably torsade de pointes. Others
are ventricular tachycardia, supraventricular tachycardia and atrial fibrillation.
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.
Obstetric
Most importantly pre-eclampsia. It has an indirect antithrombotic effect upon thrombocytes and
the endothelial functions (increase in prostaglandin, decrease in thromboxane, decrease in
angiotensin II), microvascular leakage and vasospasm through its function similar to calcium
channel blockers.
Convulsions are the result of cerebral vasospasm. The vasodilatatory effect of magnesium seems
to be the major mechanism.
Electrolyte disturbances
Pulmonary
Acute asthma, here there is a bronchodilatatory effect, probably by antagonizing a calciummediated constriction. Also, adrenergic stimulation, i.e. sympatheticomimetics used for treatment
of asthma, might lower serum levels of magnesium, which must therefore be supplemented.
Sedation and anxiolytics may help in decreasing bronchoconstriction.
Sumber: http://en.wikipedia.org/wiki/Hypomagnesemia