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Monday, 16 December 2013

Magnesium deficiency

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