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How Best to Determine Magnesium Status: A New Laboratory Test Worth Trying

The article by Sacks, Brown, Dickerson and their colleagues1 considers the limitations of tests that determine magnesium status before and after magnesium therapy to restore depleted levels of ten critically ill patients identified as magnesium deficient on the basis of low serum values. Because the added risk of complications from magnesium depletion in patients already at high risk from their injuries has been cited, the authors provided a continuous 24-h intravenous infusion containing magnesium (0.5 or 0.75 mmol/kg as MgSO4). They attempted to evaluate the efficacy of treatment, not only by changes in serum values. but by white bloodcell.( mononuclear) determinations, which is considered a better index of tissue magnesium content. It was unanticipated that the mononuclear blood cell magnesium would be less indicative of response to the magnesium infusion than were the serum levels.

The authors considered several possible explanations for the failure to demonstrate repletion by this blood cell test. They suggested that variability in the assay, in conjunction with the small number of patients in their study, and a possible presumptive lowered renal threshold for magnesium reabsorption, might account for failure to retain sufficient magnesium to replete tissue levels. However, the elevation of serum magnesium levels and correction of hypocalcemia ( a consequence of magnesium depletion's impairment of parathyroid hormone secretion, which the authors cited) indicate that the infusion corrected those manifestations of magnesium deficiency. They also consider it possible that the amount of magnesium infused was insufficient to replete tissue stores in critically ill patients. All these points are valid, but caution must be exercised in increasing the magnesium load in a 24-h infusion to avoid levels that might produce hypermagnesemia. Patients with decreased renal reabsorption of magnesium would be at low risk of hypermagnesemia. Patients with impaired renal clearance would be at high risk of high circulating magnesium, which can cause sufficient peripheral vasodilatation to trigger hypotension and even shock, and might slow cardiac conduction, with risk of bradycardia and even heart block.2,3 Abbott and Rude4 have found lower infusion doses of parenteral magnesium (12-24 mmol mg/d) given for 3-5 d, followed by long-term repletion with orally administered magnesium (300-600 mg/d), to be effective in repairing magnesium deficiency, even when characterized by acute signs, in critically ill patients.

Whether the measurement of blood cell magnesium is necessarily the best test to evaluate response to magnesium infusion is uncertain. Arnold et al.5 evaluated the magnesium status in erythrocytes and mononuclear blood cells in 15 critically ill patients whose magnesium depletion had been diagnosed by the magnesium-load test. They found no significant difference in plasma, red cell, and mononuclear blood cell magnesium levels between magnesium depleted and nondepleted groups, and concluded that a diagnosis of magnesium depletion cannot be excluded despite normal values in plasma, erythrocytes, or mononuclear blood cells.

In the serum magnesium test, the more indicative of those used by Sacks et al.,1 serum magnesium comprises only 0.3% of the body's magnesium (of about 24 g or 1 mol) and is made up of protein-bound, complexed, and free ionic magnesium, which constitutes 71 % of the amount in serum, and is the fraction that is biologically active.6,7 There are now several ion-selective electrode (ISE) instruments that are commercially available.7-10 Which of the devices is best to use is still controversial. The prototype of the NOVA Biomedical instrument, used by Altura and colleagues,7,10,11 has provided the most data. They have found that their ISE is selective for Mg2+, and exhibits little or no interference from pathophysiologic concentrations of ionic calcium, sodium, potassium, hydrogen, ammonium, or heavy metals (e.g., ionic iron, copper, zinc, cadmium, mercury, or lead) in serum. Importantly, silicon (as found in vacutainer tubes) does not interfere with measured levels — an important attribute in collecting and transporting samples for analysis. Using this device, Altura et al.7,11,12 have found [Mg2+]o to be 71% of the total magnesium in serum, it varies from subject to subject, but has been remarkably consistent in sequential samples from an individual. Use of specific ISEs for [Mg2+]o has disclosed that Mg2+ levels often exhibit significant differences from normality, despite no change in total serum magnesium in many disorders (i.e., cardiac disease, hypertension, cardiopulmonary bypass, abnormal pregnancy, renal and hepatic transplant, migraine headaches, head injury, stroke, diabetes, asthma, and other conditions).

Estimation of the [Mg2+]o level in serum or plasma by analysis of ultrafiltrates (complexed Mg + Mg2+) is somewhat unsatisfactory and time consuming. More importantly, these methods do not distinguish the ionized or free form of Mg from the Mg2+ bound to organic and inorganic anions.11-13 Because the levels of these ligands (e.g., lactate, bicarbonate, sulfate, citrate, phosphate, acetate, etc.) can vary significantly in numerous pathologic states, it is desirable to measure the levels of Mg2+ directly, in complex matrices such as whole blood, plasma, and serum. Virtually no difference in [Mg2+]o was found using the novel ISE, irrespective of whether whole blood, plasma, or serum was sampled.7,10,13 These data demonstrate that the mean concentration of [Mg2+]o in human blood is about 600 µmol/L (0.54-0.65 mM/L, 95% CI), with 65-72% total Mg being free or biologically active. Use of 3lP-nuclear magnetic resonance spectroscopy on human red blood cells in samples taken from patients with disease states to measure tissue intracellular free Mg ([Mg2+]i demonstrate a high correlaton (r = 0.5-0.8; P < 0.01) between [Mg2+]o and [Mg2+]i, suggesting that a Mg2+ measurement might be, quantitatively, a "true reflection" of soft tissue levels.14,15

Difficulties in diagnosing magnesium deficiency and in evaluating response to therapy are largely to blame for delays in accepting low serum magnesium as an important contributor to morbidity and mortality, and in attempting to correct it, a particlarly important variable in the critically ill. Now that clinically available means to determine ionic magnesium levels are more widely available, the substantial knowledge of the importance of diagnosing magnesium deficiency in patients, determining the effects of drugs that affect its levels, and ascertaining success in its repletion should be increasingly applied to patient care.

Decatur, Georgia, USA

Department of Physiology
SUNY Health Science Center at Brooklyn
Brooklyn, New York, USA


1. Sacks GS. Brown RO. Dickerson RN. et al.. Mononuclear blood cell magnesium content and serum magnesium concentration in critically ill hypomagnesemic patients after replacement therapy. Nutrition 1997; 13:303

2. Altura BM, Altura BT. Magnesium, electrolyte transport, and coronary vascular tone. Drugs 1984;28 (suppl. 1):120

3. Seelig MS, Elin RJ, Antman EM. Magnesium in acute myocardial infarction: still an open question. (submitted for publication)

4. Abbott LG, Rude RK. Clinical manifestations of magnesium deficiency. Miner Electrolyte Metab 1993; 19:314

5. Arnold A, Tovey J, Mangat P, Penny W, Jacobs S. Magnesium deficiency in critically ill patients. Anaesthesia 1995;50:203

6. Elin RJ. Assessment of magnesium status. In: Itokawa Y, Durlach J, eds. Magnesium in health and disease. London: J. Libbey, 1989:137

7. Altura BT, Altura BM. Measurement of ionized magnesium in whole blood, plasma and serum with a new ion-selective electrode in healthy and diseased human subjects. Magnes Trace Elem 1991-1992;10:90

8. Lewenstam A, Blomqvist N, Ost J. Characterization, standardization and experiences with KONE ISE for Mg2+. Scand J Clin Lab Invest 1994;54(suppl. 217):37

9. Altura BM, Lewestam A. Unique magnesium-sensitive ion selective electrodes. Scand J Clin Lab Invest 1994;54(Suppl. 217):1

10. Altura BT, Bertschat F, Jeremias A, Ising H, Altura BM. Comparative findings on serum Mg2+ of normal and diseased human subjects with rhe NOY A and KONE ISE's for Mg2+. Scand J Clin Lab Invest 1994;54(suppl. 217):77

11. Altura BT, Altura BM. Role of magnesium in pathophysiological processes and the clinical utility of magnesium ion selective electrodes. Scand J Clin Lab Invest 1996;56(suppl. 224):211

12. Altura BT, Shirey TL, Young CC, et al. Characterization of a new ion selective electrode for ionized magnesium in whole blood, plasma, serum, and aqueous samples. Scand J Clin Lab Invest 1994;54(suppl. 217):21

13. Altura BT, Altura BM. A method for distinguishing ionized, complexed and protein-bound Mg in normal and diseased subjects. Scand J Clin Lab Invest 1994;54(suppl. 217):83

14. Altura BT, Burack JL, Cracco RQ, et al. Clinical studies wirh the NOVA ISE for IMg2+. Scand J Clin Lab Invest 1994; 54 (suppl. 217):53

15. Altura BM, Altura BT. Magnesium in cardiovascular biology. Scientific Am Sci Med 1995:28-30.

PH S0899-9007(97)00073-7

Nutrition 13 (1997):376-377

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