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Within 1 day
Turnaround time is defined as the usual number of days from the date of pickup of a specimen for testing to when the result is released to the ordering provider. In some cases, additional time should be allowed for additional confirmatory or additional reflex tests. Testing schedules may vary.
Serum (preferred) or plasma
0.5 mL (Note: This volume does not allow for repeat testing.)
Red-top tube, gel-barrier tube, or green-top (lithium heparin) tube
Separate serum or plasma from cells within 45 minutes of collection.
Maintain specimen at room temperature.
EDTA or citrate plasma specimen
Magnesium deficiency produces neuromuscular disorders. It may cause weakness, tremors, tetany, and convulsions. Hypomagnesemia is associated with hypocalcemia, hypokalemia, long-term hyperalimentation, intravenous therapy, diabetes mellitus, especially during treatment of ketoacidosis; alcoholism and other types of malnutrition; malabsorption; hyperparathyroidism; dialysis; pregnancy; and hyperaldosteronism. Renal loss of magnesium occurs with cis-platinum therapy. Alfrey also adds amphotericin toxicity to the causes of hypomagnesemia.
Magnesium deficiency is described with cardiac arrhythmias. The concept that magnesium deficiency may cause arrhythmias is repeatedly expressed.
Increased magnesium levels relate mostly to patients in renal failure. Marked increases may be found in such patients who take magnesium salts (eg, as antacids which contain magnesium). Increased serum magnesium is also found with Addison disease and in pregnant patients with severe preëclampsia or eclampsia who are receiving magnesium sulfate as an anticonvulsant. Hypermagnesemia may occur in patients using magnesium-containing cathartics.1 High magnesium levels are manifested by decreased reflexes, somnolence, and heart block.2
Indications for measurement of serum magnesium include the presence of unexplained hypocalcemia, instances in which hypokalemia is unresponsive to potassium supplementation, and in patients who have cardiac disorders in which hypomagnesemia may be especially hazardous such as congestive failure, ventricular ectopy, digitalis use, or left ventricular hypertrophy. Serum magnesium is indicated only selectively in patients on diuretics: those on high dose thiazides, loop diuretics or hydrochlorothiazide in doses >50 mg/day.3
Because an association between aminoglycoside therapy and severe hypomagnesemia is described, a recommendation is published to measure serum magnesium in subjects receiving aminoglycosides. Recommendations also exist to measure it in patients on cyclosporine.4,5
Hemolysis will yield elevated results as levels in erythrocytes are two to three times higher than serum. Bilirubin may cause falsely low values.6
Parathormone enhances tubular reabsorption of magnesium. Measure magnesium in patients with hypocalcemia, of whom 23%, without renal failure, were found in one study to have hypomagnesemia.2 Magnesium containing drugs can cause toxic levels in patients with impaired renal function. A causal relation between decreased Mg2+ content of cardiac muscle/coronary arteries and nonocclusive sudden-death ischemic heart disease has been proposed. Serum magnesium constitutes only a small fraction of total body stores and may not predict magnesium status correctly.7 Magnesium acts as a metallic cofactor in over 300 enzymatic reactions.8 A positive correlation between normomagnesemia and successful resuscitation is reported.9 Serum magnesium has prognostic importance in congestive heart failure.10
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