Magnesium
Magnesium is the eleventh most abundant element by mass in the human
body. The adult body content is 25 g distributed in the skeleton and
soft tissues. The chemical is essential in manipulating important
biological polyphosphate such as ATP, DNA, and RNA and in functionming
enzymes(a).
1. Magnesium metabolism and its disorders
Magnesium is the fourth most abundant cation in the body and plays an important physiological role in many of its functions. Magnesium balance is maintained by renal regulation of magnesium reabsorption. According to the study by the Department of Chemical Pathology, St Thomas' Hospital, magnesium deficiency and hypomagnesaemia can result from a variety of causes including gastrointestinal and renal losses. Magnesium deficiency can cause a wide variety of features including hypocalcaemia, hypokalaemia and cardiac and neurological manifestations. Chronic low magnesium
state has been associated with a number of chronic diseases including
diabetes, hypertension, coronary heart disease, and osteoporosis. The
use of magnesium
as a therapeutic agent in asthma, myocardial infarction, and
pre-eclampsia is also discussed. Hypermagnesaemia is less frequent than
hypomagnesaemia and results from failure of excretion or increased
intake. Hypermagnesaemia can lead to hypotension and other
cardiovascular effects as well as neuromuscular manifestations(1).
2. Implications of magnesium deficiency in type 2 diabetes
Magnesium is
the fourth most abundant cation in the body and plays an important
physiological role in many of its functions. It plays a fundamental role
as a cofactor in various enzymatic reactions involving energy
metabolism. According to the study by the Punjab Agricultural University, magnesium is a cofactor of various enzymes in carbohydrate oxidation and plays an important role in glucose transporting mechanism of the cell membrane. It is also involved in insulin secretion, binding, and activity. Magnesium deficiency and hypomagnesemia can result from a wide variety of causes, including deficient magnesium intake, gastrointestinal, and renal losses. Chronic magnesium deficiency has been associated with the development of insulin resistance. The present review discusses the implications of magnesium deficiency in type 2 diabetes(2).
3. Magnesium (Mg) status in patients with cardiovascular diseases
Mg is an important cofactor for many enzymes especially those involved
in phosphate transfer reactions. Mg is therefore essential in the
regulation of the metabolism of other ions and cellular functionsé According to the study by the, deficiency
has
been shown to be associated with fatal cardiovascular diseases such as
cardiac arrhythmias and coronary heart disease, as well as with risk
factors for these diseases, such as hypertension, and diabetes mellitus.
Our findings showed that serum total Mg was similar in all groups, but
patients with arrhythmias and diabetes mellitus revealed lower levels of
serum ionized Mg. On the other hand, patients with essential
hypertension exhibited higher intraerythrocyte Mg concentrations than
healthy controls(3).
4. Hypokalemia and hypomagnesemia in a cirrhotic patient. Correction of metabolic disorders by magnesium
According to the study by Bletry O, Certin M, Herreman G, Wechsler B, and Godeau P., there is a report of a case of a cirrhotic with severe hypokalemia (2 mEq/l) responding incompletely to attempts at correction by classical treatments. The findings of a serum and red cell magnesium deficiency led to administration of this electrolyte which proved efficacous. They then recall the mechanism of hypokalemia
and hypomagnesemia in alcoholics, study the possible relationship
between these abnormalities, their noxious effects and suggest a
treatment(4).
5. Symptomatic hypomagnesemia in children
Hypocalcemia and hyperphosphatemia suggesting impaired parathyroid function were the most common electrolyte disorders. Hypokalemia
was also frequently noted. The related symptoms including seizure,
tetany, and weakness were common. According to the National Taiwan
University Hospital, hypocalcemia and hyperphosphatemia suggesting
impaired parathyroid function were the most common electrolyte
disorders. Hypokalemia was also frequently noted. The related symptoms including seizure, tetany, and weakness were common. Drug-induced renal magnesium
wasting was the most common cause of symptomatic hypomagnesemia, and
tended to occur in older children using aminoglycoside, furosemide, and
amphotericin-B. The associated gastrointestinal causes might add a minor
contribution to the development of hypomagnesemia. Analyses of PTH
levels in 13 children suggested that inhibition of PTH synthesis or
secretion was responsible for hypomagnesemic hypocalcemia in most
patients. However, peripheral PTH resistance might also account for the mechanism in a few patients. In most patients, symptomatic hypomagnesemia was transient, and improved after magnesium provision. Only one child with congenital renal magnesium wasting and two with primary hypomagnesemia needed long-term magnesium treatment(5).
6. Hypomagnesemia: an evidence-based approach to clinical cases
Hypomagnesemia is defined as a serum magnesium level less than 1.8 mg/dL (< 0.74 mmol/L). Hypomagnesemia may result from inadequate magnesium
intake, increased gastrointestinal or renal losses, or redistribution
from extracellular to intracellular space. Increased renal magnesium
loss can result from genetic or acquired renal disorders. According to
the Rush University Medical Center, Chicago, most patients with
hypomagnesemia are asymptomatic and symptoms usually do not arise until
the serum magnesium
concentration falls below 1.2 mg/dL. One of the most life-threatening
effects of hypomagnesemia is ventricular arrhythmia. The first step to
determine the likely cause of the hypomagnesemia is to measure
fractional excretion of magnesium and urinary calcium-creatinine ratio. The renal response to magnesium deficiency due to increased gastrointestinal loss is to lower fractional excretion of magnesium to less than 2%. A fractional excretion above 2% in a subject with normal kidney function indicates renal magnesium
wasting. Barter syndrome and loop diuretics which inhibit sodium
chloride transport in the ascending loop of Henle are associated with hypokalemia, metabolic alkalosis, renal magnesium
wasting, hypomagnesemia, and hypercalciuria. Gitelman syndrome and
thiazide diuretics which inhibit sodium chloride cotransporter in the
distal convoluted tubule are associated with hypokalemia, metabolic alkalosis, renal magnesium wasting, hypomagnesemia, and hypocalciuria. Familial renal magnesium
wasting is associated with hypercalciuria, nephrocalcinosis, and
nephrolithiasis. Asymptomatic patients should be treated with oral magnesium supplements. Parenteral magnesium should be reserved for symptomatic patients with severe magnesium deficiency (< 1.2 mg/dL). Establishment of adequate renal function is required before administering any magnesium supplementation(6).
7. Abnormal renal magnesium handling
The normal fractional urinary excretion of filtered magnesium is about 5%. In magnesium deficiency in man, the kidneys can normally reduce the 24-hour urinary magnesium excretion to less than 1 mmol (24 mg) via unknown mechanisms, and initially without a fall in plasma magnesium concentration. According to the University of British Columbia, congenital renal magnesium
wasting occurs in several syndromes including Bartter's syndrome in
which it is associated with hypercalciuria, and the defect may be in the
thick ascending limb of Henle's loop, and Gitelman's syndrome in which
there is hypocalciuria, and the defect may be in the distal convoluted
tubule. Other causes of renal magnesium wasting include diabetes mellitus, hypercalcemia and diuretics. Magnesium
wasting may also result from various toxicities including those of
cis-platinum, in which the biochemical features resemble Gitelman's
syndrome, and those of aminoglycosides, pentamidine and cyclosporin.
Calcitriol deficiency may also contribute to renal magnesium
wasting in some circumstances. Mild hypermagnesemia may occur in
familial hypocalciuric hypercalcemia and may reflect abnormal
sensitivity of the loop of Henle to calcium and magnesium ions. By contrast, the hypermagnesemia that occurs in chronic renal failure results from the reduced glomerular filtration of magnesium(7).
8. Hypomagnesemia: renal magnesium handling
Magnesium is an important constituent of the intracellular space that affects a number of intracellular and whole body functions. Magnesium
balance depends on intake and renal excretion, which is regulated
mainly in the thick ascending limb of the loop of Henle. According to
the University of Pennsylvania School of Medicine, hypomagnesemia may
result from gastrointestinal losses or renal losses, the latter due to
primary renal magnesium wasting or in association with sodium loss. Hypomagnesemia may arise together with and contribute to the persistence of hypokalemia
and hypocalcemia. The major direct toxicity of hypomagnesemia is
cardiovascular. When urgent correction of hypomagnesemia is required, as
with myocardial ischemia, post cardiopulmonary bypass, and torsades de
pointes, intravenous or intramuscular magnesium sulfate should be used. Oral magnesium preparations are available for chronic use(8).
9. Magnesium metabolism in health and disease
Magnesium (Mg)
is the main intracellular divalent cation, and under basal conditions
the small intestine absorbs 30-50% of its intake. Normal serum Mg ranges
between 1.7-2.3 mg/dl (0.75-0.95 mmol/l), at any age. According to the
study by Hospital Italiano de Buenos Aires, eEven though eighty percent
of serum Mg is filtered at the glomerulus, only 3% of it is finally
excreted in the urine. Altered magnesium
balance can be found in diabetes mellitus, chronic renal failure,
nephrolithiasis, osteoporosis, aplastic osteopathy, and heart and
vascular disease. Three physiopathologic mechanisms can induce Mg deficiency:
reduced intestinal absorption, increased urinary losses, or
intracellular shift of this cation. Intravenous or oral Mg repletion is
the main treatment, and potassium-sparing diuretics may also induce
renal Mg saving. Because the kidney has a very large capacity for Mg
excretion, hypermagnesemia usually occurs in the setting of renal
insufficiency and excessive Mg intake. Body excretion of Mg can be
enhanced by use of saline diuresis, furosemide, or dialysis depending on
the clinical situation(9).
10. Magnesium deficiency: pathogenesis, prevalence, and clinical implications
Hypomagnesemia is probably the most underdiagnosed electrolyte deficiency in current medical practice. Patients with cardiovascular disease who are at greatest risk for the development of magnesium deficiency are those treated with diuretics or digitalis. According to the study by the, both potassium and magnesium
deficiencies are associated with increased ventricular ectopy and may
increase the risk of sudden unexpected death. Refractory potassium
repletion can be caused by concomitant magnesium depletion, and can be corrected with magnesium supplementation. Routine serum magnesium
determination is recommended whenever the testing of electrolyte levels
is required, especially in patients taking diuretic drugs or digitalis.
Because hypomagnesemia is not necessarily present in a magnesium-deficient state, it is recommended that both potassium and magnesium be repleted in patients with hypokalemia. Potassium-/magnesium-sparing diuretics may be helpful in the prevention of these electrolyte deficiencies(10).
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Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/18568054
(2) http://www.ncbi.nlm.nih.gov/pubmed/19629403
(3) http://www.ncbi.nlm.nih.gov/pubmed/10375959
(4) http://www.ncbi.nlm.nih.gov/pubmed/198892
(5) http://www.ncbi.nlm.nih.gov/pubmed/9926514
(6) http://www.ncbi.nlm.nih.gov/pubmed/20081299
(7) http://www.ncbi.nlm.nih.gov/pubmed/8264509
(8) http://www.ncbi.nlm.nih.gov/pubmed/9459289
(9) http://www.ncbi.nlm.nih.gov/pubmed/19274487
(10) http://www.ncbi.nlm.nih.gov/pubmed/3565424
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