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PubMedDate not supplied

Magnesium in disease: a review with special emphasis on the serum ionized magnesium.

This review deals with the six main clinical situations related to magnesium or one of its fractions, including ionized magnesium: renal disease, hypertension, pre-eclampsia, diabetes mellitus, cardiac disease, and the administration of therapeutic drugs. Issues addressed are the physiological role of magnesium, eventual changes in its levels, and how these best can be monitored. In renal disease mostly moderate hypermagnesemia is seen; measuring ionized magnesium offers minimal advantage. In hypertension magnesium might be lowered but its measurement does not seem relevant. In the prediction of severe pre-eclampsia, elevated ionized magnesium concentration may play a role, but no unequivocal picture emerges. Low magnesium in blood may be cause for, or consequence of, diabetes mellitus. No special fraction clearly indicates magnesium deficiency leading to insulin resistance. Cardiac diseases are related to diminished magnesium levels. During myocardial infarction, serum magnesium drops. Total magnesium concentration in cardiac cells can be predicted from levels in sublingual or skeletal muscle cells. Most therapeutic drugs (diuretics, chemotherapeutics, immunosuppressive agents, antibiotics) cause hypomagnesemia due to increased urinary loss. It is concluded that most of the clinical situations studied show hypomagnesemia due to renal loss, with exception of renal disease. Keeping in mind that only 1% of the total body magnesium pool is extracellular, no simple measurement of the real intracellular situation has emerged; measuring ionized magnesium in serum has little added value at present.

Diabetes Mellitus↗

PubMed2001

Acute cardiovascular effects of magnesium and their relationship to systemic and myocardial magnesium concentrations after short infusion in awake sheep.

The temporal relationship between the systemic and myocardial concentrations of magnesium and some of its acute cardiovascular effects were examined after short i.v. infusion administration of magnesium (30 mmol over 2 min) in five awake chronically instrumented sheep. Magnesium decreased mean arterial blood pressure and systemic vascular resistance (SVR) by 23 and 41% from baseline, respectively. These hemodynamic changes were consistent with magnesium producing primary reductions in SVR with partial heart rate (HR)-mediated compensation of blood pressure. Cardiac output and HR increased by 38 and 38% from baseline, respectively. Magnesium had little effect on myocardial contractility, but substantially increased myocardial blood flow (MBF, 77% above baseline) primarily due to direct myocardial vasodilation. The peak arterial and coronary sinus serum magnesium concentrations were 6.94 +/- 0.26 (mean +/- S.E.M.) and 6.51 +/- 0.20 mM, respectively, at 2 min. Both arterial and coronary sinus magnesium concentrations at the end of the study were still more than 3 mM, whereas all the cardiovascular effects were back to baseline. The myocardial kinetics of magnesium was consistent with rapid equilibration of magnesium (half-life 0.4 min) with a small distribution volume (71 ml) consistent with the extracellular space of the heart. In conclusion, magnesium was shown to have a rapid equilibration between the plasma/serum concentrations of magnesium and its extracellular concentration in the myocardium. However, the primary cardiovascular effect of magnesium (reductions in SVR) preceded its extracellular concentrations, and was a direct function of its arterial concentration. A "threshold" model for changes in SVR was preferred when linked to the arterial magnesium concentration.

Animals↗

PubMed2004

Changes in erythrocyte contents of potassium, sodium and magnesium and Na, K-pump activity after the administration of potassium and magnesium salts.

Low potassium and magnesium status and decreased Na, K-pump activity is an endemic condition among rural Northeast Thais. The authors examined the effect of supplementing potassium and magnesium on erythrocyte potassium, sodium and magnesium content and on Na, K-pump activity. Rural Northeast Thai renal stone patients (62) were recruited, divided into four groups and supplemented for one month with potassium chloride (Group1, n = 16), potassium-sodium citrate (Group2, n = 15), chelated magnesium (Group 3, n =16) and potassium-magnesium citrate (Group 4, n =15) in order to achieve 40 mmol potassium, 10 mmol magnesium and 60 mmol citrate daily. After supplementation with potassium (Groups 1, 2 and 4), plasma potassium and Na, K-pump activity rose significantly in Groups 1, 2 and 4, but erythrocyte potassium rose only in Groups 2 and 4. When supplementing elemental magnesium (Groups 3 and 4), the chelated magnesium caused a significant increase in plasma potassium, erythrocyte potassium, sodium and magnesium without a significant increase in Na, K-pump activity. By contrast, potassium-magnesium citrate caused a significant increase in erythrocyte potassium and magnesium and Na, K-pump activity, but depressed erythrocyte sodium. These results suggest the forms of potassium and /or magnesium salts being supplemented should be considered because they affect erythrocyte potassium, sodium and magnesium content and Na, K-pump activity differently.

Erythrocytes↗

PubMed1993

Laboratory evaluation of magnesium status. Renal function and free intracellular magnesium concentration.

In summary, magnesium plays an essential role in both extracellular and intracellular metabolism. Even though biologists recognize the importance of magnesium, clinicians often are unaware of the frequency and significance of magnesium disturbances. Some clinicians recommend routine measurement of magnesium when other electrolyte analyses are required for the care of patients. Others have reported a high frequency of hypomagnesemia in hospitalized patients, but the clinical significance of this observation was not evident. Patients with coexisting hypokalemia of any cause require particular attention however, and it is important to assess magnesium status in that setting. The assessment of magnesium status is difficult because of the distribution of magnesium within the intracellular compartment. The majority of body magnesium is located within soft and hard tissues and most intracellular magnesium is complexed and not available for measurement. Accordingly, no single determination is available to accurately assess magnesium status. The simplest and most useful approach is the determination of serum magnesium and renal magnesium clearance and interpretation of these parameters in light of complete history and clinical evaluation of the patient. Accordingly, one combines the laboratory assessment with the clinical evaluation. Other tests, such as determination of serum and intracellular free Mg2+ activity by either fluorescent or 31P-NMR techniques, are not particularly useful in the routine laboratory. These approaches currently are being used on an experimental basis to assess the role of magnesium in health and disease, which may lead to better indices of clinical evaluation in the future.

Humans↗

PubMed1976

Effect of fluoride on the mobilization of skeletal magnesium and soft-tissue calcinosis during acute magnesium deficiency in the rat.

To investigate the effect of fluoride on the mobilization of skeletal magnesium and on kidney calcification during magnesium depletion, male Holtzman rats were fed a magnesium-sufficient diet (400 ppm of magnesium) and drinking water containing either 0, 50 or 100 ppm of fluoride for a 20-day period prior to the initiation of magnesium deficiency. The high fluoride regimen resulted in a 100-fold increase in the fluoride content of the skeleton. On day 20 magnesium depletion was initiated by feeding the animals a diet containing 12 ppm of magnesium. Over a 4-week period of magnesium deprivation, a 26% decrease of the total magnesium in the humeri was observed. Fluoride exerted a significant effect in retarding the mobilization of skeletal magnesium. Four weeks of magnesium deficiency was associated with a decreased rate of skeletal mineral accretion and with an increase in the kidney calcium content. The decreased rate of mineral accretion was accentuated by the administration of fluoride during the deficiency state. While fluoride exerted an initial protective effect on calcinosis of the kidneys, the overall effect of the administration of fluoride during magnesium deficiency was to promote calcification of the kidneys rather than to prevent it.

Animals↗

PubMedDate not supplied

Intravenous magnesium sulfate relieves cluster headaches in patients with low serum ionized magnesium levels.

Patients with cluster headaches have been reported to have low serum ionized magnesium levels. We examined the possibility that patients with cluster headaches and low ionized magnesium levels may respond to an intravenous infusion of magnesium sulfate. Thirty-eight infusions of magnesium sulfate were given to 22 patients with cluster headaches. The mean ionized magnesium level prior to 23 infusions which provided relief for at least 2 days and enabled the patient to skip two or more attacks, was 0.521 +/- 0.016 mmol/L; this value was 0.561 +/- 0.016 prior to 15 infusions which were ineffective. These latter 15 infusions were preceded by higher total magnesium levels. The ionized magnesium level prior to the 23 effective infusions was below 0.54 mmol/L in 19 patients. Five of the 15 ineffective infusions were accompanied by basal ionized magnesium levels below 0.54 mmol/L. In 76% of the infusions, there was a correlation between a response and an ionized magnesium level below 0.54 mmol/L. Nine patients (41%) obtained clinically meaningful improvement. Spontaneous remissions and a placebo effect might have accounted for some of the improvement. However, this should have applied equally to all patients, regardless of the ionized magnesium level. Measurements of ionized magnesium may prove useful in elucidating the pathogenesis of cluster headache and in identifying patients who may benefit from treatment with magnesium.

Adult↗

PubMed1987

Effect of magnesium salt anions on potassium balance in normal and magnesium-depleted rats.

Potassium depletion often accompanies clinically significant magnesium depletion, and magnesium replacement is most frequently undertaken with magnesium sulfate. However, inorganic sulfate acts as a nonreabsorbable anion in the distal nephron, an effect that could potentially interfere with the correction of any associated potassium deficiency. We have investigated the effect of a variety of magnesium salts, including sulfate and nonsulfate forms, on cation balance and skeletal muscle ion composition in normal and magnesium-depleted rats. Even modest amounts of dietary sulfate increased the urinary excretion of potassium in both normal and magnesium-depleted rats. During a 7-day feeding period, diets containing MgSO4 or MgO with an equivalent amount of Na2SO4 resulted in significantly greater urinary excretion of potassium than diets without sulfate. In normal animals, this kaliuresis did not produce hypokalemia or muscle potassium depletion. Magnesium-deficient feeding produced magnesium depletion, kaliuresis, and a decline in both plasma and muscle potassium content. When magnesium was restored to the diet without sulfate, urinary potassium excretion decreased, and both magnesium and potassium deficits were corrected. However, when magnesium refeeding included sulfate salts, magnesium stores returned to normal, whereas the kaliuresis and potassium depletion persisted. When accompanied by a high sodium intake, the kaliuretic effect of sulfate was increased.

Animals↗

PubMed1951