Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.
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PMID:Magnesium deficiency and cardiac disorders. 80 29

Magnesium, the second most abundant intracellular cation, is essential for life. The consequences of deficiency are severest in the smallest and youngest members of each species and may include sudden unexpected death. Magnesium deficiency, usually diagnosed by hypomagnesemia, may be congenital, as in premature infants, infants of magnesium-deficient mothers and infants with intrauterine growth retardation. It may be acquired or caused by low magnesium intake, the use of magnesium-wasting drugs, illness provoking gastrointestinal or renal losses of the mineral, or high metabolic demands imposed by catch-up growth or postsurgical healing. Finally, the deficiency may be conditioned, caused by excessive dietary calcium, phosphorus or protein in relation to dietary magnesium, especially during a period of rapid growth or tissue repair. Magnesium therapy is safe when a low dosage is given with monitoring of plasma or serum magnesium levels, with occasional checking of calcium and potassium levels. A parenteral dose of 0.1 ml/kg/day of 50% magnesium sulfate USP (approx. 0.2 mmol/kg/day or 0.4 mEq/kg/day) may be given for 5 dose days. An oral dose of 1.0 ml of 10% magnesium chloride solution providing 0.5 mmol/kg/day magnesium or 1.0 ml/kg/day of 10% magnesium chloride USP (0.5 mmol/kg/day) or magnesium magonate (Magonate) 1.0 ml/kg/day (0.45 mmol/kg/day) may be given for extended periods; higher doses may be required for malabsorption syndromes. Hypermagnesemia, which usually results from magnesium overdosage or inadequate renal function, is a potential threat to neonates born to magnesium-treated eclamptic mothers. Most show marked improvement after 36 h of conservative management that includes calcium salts and intravenous infusions of glucose and saline, but obtunded neonates may require dialysis.
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PMID:Magnesium in perinatal care and infant health. 184 56

Magnesium is an important element for health and disease. Magnesium, the second most abundant intracellular cation, has been identified as a cofactor in over 300 enzymatic reactions involving energy metabolism and protein and nucleic acid synthesis. Approximately half of the total magnesium in the body is present in soft tissue, and the other half in bone. Less than 1% of the total body magnesium is present in blood. Nonetheless, the majority of our experimental information comes from determination of magnesium in serum and red blood cells. At present, we have little information about equilibrium among and state of magnesium within body pools. Magnesium is absorbed uniformly from the small intestine and the serum concentration controlled by excretion from the kidney. The clinical laboratory evaluation of magnesium status is primarily limited to the serum magnesium concentration, 24-hour urinary excretion, and percent retention following parenteral magnesium. However, results for these tests do not necessarily correlate with intracellular magnesium. Thus, there is no readily available test to determine intracellular/total body magnesium status. Magnesium deficiency may cause weakness, tremors, seizures, cardiac arrhythmias, hypokalemia, and hypocalcemia. The causes of hypomagnesemia are reduced intake (poor nutrition or IV fluids without magnesium), reduced absorption (chronic diarrhea, malabsorption, or bypass/resection of bowel), redistribution (exchange transfusion or acute pancreatitis), and increased excretion (medication, alcoholism, diabetes mellitus, renal tubular disorders, hypercalcemia, hyperthyroidism, aldosteronism, stress, or excessive lactation). A large segment of the U.S. population may have an inadequate intake of magnesium and may have a chronic latent magnesium deficiency that has been linked to atherosclerosis, myocardial infarction, hypertension, cancer, kidney stones, premenstrual syndrome, and psychiatric disorders. Hypermagnesemia is primarily seen in acute and chronic renal failure, and is treated effectively by dialysis.
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PMID:Magnesium metabolism in health and disease. 328 51