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MGU
8595
potassium, chloride, and sulfate are usually the major contributors to fecal osmolality. Fecal osmolality is
normally 2 x (sodium + potassium) unless there are exogenous factors inducing a change in this ratio,
such as the presence of other osmotic agents (magnesium sulfate, saccharides), or drugs inducing
secretions, such as phenolphthalein or bisacodyl. If magnesium is excreted at a high rate (>30 mEq/24
hour), with an osmotic gap >100 mOsm/kg, magnesium is likely to be the principle contributor to osmotic
diarrhea. Use of magnesium salts in the form of over-the-counter stool softeners is the most likely source
of such excess excretion.
Useful For: Diagnosis of osmotic diarrhea due to excessive ingestion of magnesium Ruling out
excessive ingestion of magnesium in the work-up of chronic diarrhea
Interpretation: The osmotic theory of diarrhea is explained by the equation: 2x (stool sodium + stool
potassium) = stool Osmolality + or - 30 mOsm. Normal fecal sodium and potassium in the presence of an
osmotic gap (>30 mOsm/kg) suggests osmotic diarrhea. Ingestion of more than usual dietary magnesium
leading to increased excretion of fecal magnesium contributes to osmotic diarrhea. Magnesium excretion
at >30 mEq/24 hour is frequently associated with decreased fecal sodium and potassium, and is an
indicator of excessive consumption of magnesium that is likely the cause of diarrhea.
Reference Values:
0-15 years: not established
> or =16 years: 0-29 mEq/24 hour
Clinical References: 1. Phillips S, Donaldson L, Geisler K, et al: Stool composition in factitial
diarrhea: a 6-year experience with stool analysis. Ann Intern Med 1995;123:97-100 2. Ho J, Moyer T,
Phillips S: Chronic diarrhea: the role of magnesium. Mayo Clin Proc 1995;70:1091-1092 3. Fine KD,
Santa Ana CA, Fordtran JS : Diagnosis of magnesium-induced diarrhea. N Engl J Med
1991;324:1012-1017
Magnesium, 24 Hour, Urine
Clinical Information: Magnesium, along with potassium, is a major intracellular cation. Magnesium
is a cofactor of many enzyme systems. All adenosine triphosphate (ATP)-dependent enzymatic reactions
require magnesium as a cofactor. Approximately 70% of magnesium ions are stored in bone. The
remainder is involved in intermediary metabolic processes; about 70% is present in free form, while the
other 30% is bound to proteins (especially albumin), citrates, phosphate, and other complex formers. The
serum magnesium level is kept constant within very narrow limits. Regulation takes place mainly via the
kidneys, primarily in the ascending loop of Henle. Conditions that interfere with glomerular filtration
result in retention of magnesium and, hence, elevation of serum concentrations. Hypermagnesemia is
found in acute and chronic renal failure, magnesium overload, and magnesium release from the
intracellular space. Mild-to-moderate hypermagnesemia may prolong atrioventricular conduction time.
Magnesium toxicity may result in central nervous system (CNS) depression, cardiac arrest, and
respiratory arrest. Numerous studies have shown a correlation between magnesium deficiency and
changes in calcium-, potassium-, and phosphate-homeostasis, which are associated with cardiac disorders
such as ventricular arrhythmias that cannot be treated by conventional therapy, increased sensitivity to
digoxin, coronary artery spasms, and sudden death. Additional concurrent symptoms include
neuromuscular and neuropsychiatric disorders. Conditions associated with hypomagnesemia include
chronic alcoholism, childhood malnutrition, lactation, malabsorption, acute pancreatitis, hypothyroidism,
chronic glomerulonephritis, aldosteronism, and prolonged intravenous feeding.
Useful For: Assessing the cause of abnormal serum magnesium concentrations Determining whether
the body is receiving adequate nutrition
Interpretation: With normal dietary intake of 200 mg to 500 mg of magnesium per day, urine
excretion is typically 75 mg/24 hours to 150 mg/24 hours. The remainder of the dietary intake passes
through the gastrointestinal tract and is excreted in the feces. Decreased renal function, such as in
dehydration, diabetic acidosis, or Addison's disease, results in reduced output of magnesium. Poor diet
(alcoholism), malabsorption, and hypoparathyroidism result in low urine magnesium due to low uptake
from the diet. Chronic glomerulonephritis, aldosteronism, and drug therapy (cyclosporine, thiazide
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