Chemical formula: C₈H₁₂MgN₂O₈ Molecular mass: 360.555 g/mol
Magnesium is a cofactor in >300 enzymatic reactions. It acts as an essential co-factor for all ATP-binding enzymes.
Magnesium plays an important role in cellular electrolyte homeostasis and in the neuromuscular membrane stabilization.
Magnesium:
Intestinal absorption is not directly proportional to magnesium intake but is dependent mainly on magnesium status. The lower the magnesium level, the more magnesium is absorbed in the gut: thus, relative magnesium absorption is high when intake is low and vice versa.
Magnesium is slowly and incompletely absorbed – primarily in the small intestine. The non-absorbable portion can produce a laxative effect.
Peak serum levels are reached after 2-3 hours. At 6h, magnesium absorption is approximately 80% complete.
Magnesium is the main intracellular divalent cation, and the normal adult human body content is around 22.6g. About 60% of the magnesium is present in bone, of which 30% is exchangeable and functions as a reservoir to stabilise the serum concentration. About 20% is in skeletal muscle, 19% in other soft tissues and less than 1% in the extracellular fluid.
After oral administration the distribution of magnesium within the body depends on the filling state of magnesium levels in each individual case. The classical method of determining bioavailability using plasma concentration curves cannot be applied to magnesium.
The concentration of magnesium in the blood serum is subject to variations during the day. Due to the equilibrium between magnesium concentration in the blood serum and the depot in the bones, no conclusions concerning the depot in the body can be drawn from the concentration of magnesium in the blood serum. Neuromuscular hyper-excitability can be an indicator of magnesium deficiency.
Absorbed magnesium is practically only secreted via the kidney.
Diuretics (e.g. thiazide, furosemide) are widely used in the treatment of hypertension, heart failure and kidney diseases. They increase urinary output with hypermagnesuria probably leading to hypomagnesaemia and magnesium depletion.
EGF-receptor antagonist (e.g. cetuximab, erlotinib) are used in the treatment of metastatic colorectal cancer. As EGF is a magnesiotropic hormone, treatment with EGF-receptor antagonists was related to severe hypomagnesaemia.
Long-term treatment with proton pump inhibitors (e.g. omeprazole, pantoprazole) has been related to severe hypomagnesaemia, probably due to disturbances in absorption.
Aminoglycoside antibiotics (e.g. gentamycin, tobramycin) are widely used in the treatment of severe bacterial infections. Studies showed that in 25% of the patients, hypomagnesaemia occurs due to renal magnesium loss.
Foscarnet is a pyrophosphate analogue that inhibits many viral DNA polymerases.
Hypomagnesaemia is among others a side effect of foscarnet treatment as foscarnet is a potent chelator of divalent cations.
Excessive excretion of magnesium into the urine is a cause of magnesium depletion. Osmotic diuresis due to glucosuria can result in magnesium depletion, and diabetes mellitus is probably the most common clinical disorder associated with magnesium depletion. Therefore, diabetics have an increased requirement for magnesium.
Magnesium deficiency has been shown to result in cardiovascular disorders such as cardiac dysrhythmias, which may be manifested by a rapid heart rate (tachycardia), skipped heart beats (premature beats), or a totally irregular cardiac rhythm (fibrillation). A low magnesium status leads to arterial vasoconstriction and thrombocyte aggregation. Migraine patients often show low magnesium levels, therefore, magnesium deficiency seems to play a role in the pathogenesis of migraine. Magnesium supplementation was effective in migraine prophylaxis.
Non-clinical data reveal no special hazard for humans based on conventional studies of safety pharmacology, repeated dose toxicity, genotoxicity, carcinogenic potential, toxicity to reproduction and development.
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