MAGNESIUM METABOLISM

This article has been published by the International Biopharmaceutical Association www.ibpassociation.org . Please note this article does not give any medical advice.

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MAGNESIUM METABOLISM

1. Over half of the body’s magnesium is stored in the bone, about 1% is found in extracellular fluid (20-30% bound to protein; the rest free) and the rest is in soft tissues, particularly muscle.
2. The kidney controls the homeostasis of magnesium.


HYPOMAGNESEMIA

Definition:
clinically significant at less than 1 mEq/L

Etiology
1. Renal causes
a. Hypercalcemia - calcium and magnesium use the same transport mechanism in the ascending loop of Henle
b. Primary tubular disorders such as Bartter’s syndrome, obstructive diuresis and renal tubular acidosis
c. Hyperaldosteronism causes magnesium losses – the mechanism is unclear.
d. Diuretics such as thiazide, furosemide and ethacrynic acid; cisplatin; gentamicin and amphotericin B
2. Extrarenal causes
a. Lack of magnesium in the diet or increased losses via the GIT due to malabsorption, chronic diarrhea or laxative abuse
b. Increased cell uptake of magnesium is associated with alcohol withdrawal syndrome. Increased storage in bone is seen after parathyroidectomy.


Manifestations:
1. Neuromuscular effects such as weakness, tremor and muscle twitches are due both to a direct effect on the neuromuscular junction and to secondary hypocalcemia.
2 Hypomagnesemia affects the reabsorption of potassium and so leads to hypokalemia. Cardiac arrhythmias may result.

Principles of management:
A normal diet is usually sufficient. Magnesium supplementation may be necessary. It is, however, not efficient since about half of what is ingested is excreted, even in the presence of severe hypomagnesemia.


HYPERMAGNESEMIA

Definition:
serum magnesium more than 2.2 mEq/L

Etiology:
1. The kidneys are capable of excreting large amounts of magnesium; hypermagnesemia is thus likely to be iatrogenic – the use of laxatives or antacids in patients with renal failure.
2 Hypermagnesemia may be seen in pregnant women with toxemia who are treated with high doses of magnesium to prevent eclampsia.

Manifestations:
At serum levels above 10 mg/dl paralysis may develop.

Principles of management:
Calcium, which acts as an antagonist of magnesium, should be administered. Dialysis may be necessary.
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