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  • Magnesium in blood serum

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    Magnesium is the fourth most element in the human body after potassium, sodium, calcium and the second most abundant element in the cell after potassium. The human body contains about 25 g of magnesium, 60% of it is part of the bone tissue, and most of the rest of the stock is in cells. Only 1% of the total magnesium is contained in the extracellular fluid. Approximately 75% of the magnesium of the serum is in ionized form, 22% is associated with albumin and 3% - with globulins. Magnesium plays an important role in the functioning of the neuromuscular apparatus. The largest content of magnesium in the myocardium. Physiologically, magnesium is a calcium antagonist, its deficiency in the serum is accompanied by an increase in the calcium content. The higher the metabolic activity of the cell, the more magnesium it contains. The concentration of ionized magnesium in the cell is maintained at a constant level even at large fluctuations of

    in its extracellular fluid. The reference values ​​of the content of magnesium in the serum of are presented in Table.[Tiz U., 1997].

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    Table Reference values ​​of magnesium concentration in blood serum

    Table Reference values ​​for magnesium concentration in blood serum

    Magnesium is a cofactor of a number of enzymatic reactions, it acts as a physiological growth regulator, supporting a stock of purine and pyrimidine bases. Magnesium is necessary at all stages of protein synthesis.

    The main regulator of maintenance of concentration of magnesium in blood serum - a kidney. In a healthy person, the daily magnesium excretion is approximately 100 mg. With the depletion of magnesium, its excretion decreases or ceases altogether. Excess magnesium is rapidly removed by the kidneys. Magnesium passes through the glomerular membrane, 80% of it is re-absorbed in the proximal tubules of the ascending segment of the Henle loop. Large doses of PTH contribute to a decrease in the excretion of magnesium in the urine( glucagon and calcitonin have the same effect).Vitamin D and its metabolites increase the absorption of magnesium in the small intestine, but to a lesser extent than calcium.

    Hypomagnesemia occurs due to the following reasons.

    ■ Reduced absorption of magnesium in the intestines due to malnutrition, impaired absorption, prolonged diarrhea. This is the mechanism of development of hypomagnesemia in acute and chronic dyspepsia, enterocolitis, ulcerative colitis, acute intestinal obstruction, edematous pancreatitis, alcoholism.

    ■ Increased magnesium excretion by kidneys due to hypercalcemia, osmotic diuresis or the administration of such drugs as loop diuretics, aminoglycosides, cyclosporine. Any damage to the renal tubules leads to an increase in the excretion of magnesium in the urine. Approximately 30% of patients with diabetes mellitus develop hypomagnesemia, but with severe forms of the disease it is difficult to detect due to a decrease in the volume of intravascular fluid. Against the background of hypomagnesemia, diabetes mellitus is more severe. The ratio of Mg / creatinine in urine in patients with diabetes mellitus increases in proportion to the severity of the clinical course of the disease.

    In clinical practice, magnesium deficiency occurs more often than it is diagnosed( approximately in 10% of inpatients).

    Magnesium - one of the regulators of vascular tone, promotes dilatation of the vascular wall. A low concentration of extracellular magnesium leads to vasospasm or increases their sensitivity to pressor agents. The intracellular magnesium content correlates with the value of arterial pressure in patients with arterial hypertension. The action of

    of a number of drugs that lower blood pressure is realized through magnesium. A decrease in the magnesium content in the myocardium was observed in the deceased from myocardial infarction and in the blood in patients with ischemic heart disease. A sharp fall in the concentration of magnesium in the blood can be one of the causes of sudden death.

    Magnesium refers to hypolipidemic agents. Hypomagnesemia contributes to the activation of the atherosclerotic process. Hyperlipidemia against hypomagnesemia promotes the progression of fatty liver infiltration. In hypomagnesemia, the activity of heparin-dependent lipoprotein lipase and lecithin cholesterol acyltransferase decreases. A violation of the clearance of LDL in a lack of magnesium explains the development of hyperlipidemia in diabetes mellitus.

    With magnesium deficiency, platelet aggregation increases, thrombogenesis processes are activated, so magnesium is considered a natural anticoagulant.

    Hypomagnesemia is a frequent complication of alcoholism and alcohol abstinence. Hypomagnesemia also accompanies hypophosphatemia( severe gipoparathyroidism and thyrotoxicosis) and intoxication with cardiac glycosides.

    When evaluating the results of a magnesium test in the blood serum, one should always remember the "false" hypomagnesemia that can be caused by stress, acute infectious diseases, hypovolemia.

    Hypomagnesemia often causes hypokalemia and hypocalcemia, which is reflected in the clinical picture. Neurological disorders include drowsiness, confusion, tremor, involuntary muscle contraction, ataxia, nystagmus, tetany, and convulsive seizures. On the ECG, the intervals PQ and QT are lengthened. Sometimes there are atrial and ventricular arrhythmias, especially in patients receiving digoxin.

    Sometimes severe cardiac arrhythmias can be corrected with magnesium preparations( with their intravenous administration), even in cases when traditional antiarrhythmic therapy is ineffective.

    It should be emphasized that it is difficult to detect magnesium deficiency( as well as its excess) in the body, which is due to its low correlation with the concentration of magnesium in the blood serum.

    Hypermagnesemia occurs in renal failure, the use of lithium drugs, hypothyroidism, lactic acidosis, hepatitis, neoplasms, the use of magnesium preparations against the background of undiagnosed renal failure. Clinical manifestations usually develop at a magnesium concentration in the serum of more than 4 meq / l. Neuromuscular disorders include areflexia, drowsiness, weakness, paralysis and respiratory failure. Cardiovascular disorders include arterial hypotension, bradycardia, prolongation of PQ, QRS and QT intervals on the ECG, complete atrioventricular block and asystole. The relationship of clinical disorders with the concentration of magnesium in the serum is as follows:

    ■ 5-10 meq / l - the delay in conducting pulses through the conduction system of the heart;

    ■ 10-13 meq / l - loss of deep tendon reflexes;

    ■ 15 meq / L - respiratory paralysis;

    ■ more than 25 meq / l - cardiac arrest in the diastole phase.