Ionized magnesium in plasma and erythrocytes for the assessment of low magnesium status in alcohol dependent patients
Michał OrdakMagdalena Maj‐ŻurawskaHalina MatsumotoMagdalena Bujalska‐ZadrożnyIlona Kieres-SalomońskiTadeusz NasierowskiElżbieta MuszyńskaMarcin Wojnar
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The kinetics of radiomagnesium exchange were measured in 9 human subjects with moderate hypomagnesemia and 1 normomagnesemic patient with demonstrated magnesium deficiency. Eight of the 10 patients were alcoholics with associated hepatic dysfunction and disturbances in the plasma concentrations of other electrolytes as well as hypomagnesemia. Three normomagnesemic patients with alcoholism and hepatic cirrhosis were also studied. A digital computer program utilizing a parallel 3-compartment open model of magnesium exchange was employed for quantitation of the primary data. At the time of study, 2–9 weeks after hospital admission, normal kinetics of magnesium exchange were found in almost all subjects. The data also indicated that conventionally calculated apparent exchangeable body pools of magnesium show a borderline correlation with computer derived values for the exchangeability of magnesium and are therefore not reliable parameters of magnesium turnover. Despite moderate hypomagnesemia and/or magnesium deficiency, the data suggest that cell membranes retain their ability to exert a control over the cellular transport of magnesium and continue to regulate the intracellular concentrations of magnesium.
Magnesium deficiency (plants)
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We observed prospectively 20 consecutive patients with severe hypomagnesemia (serum Mg 0.01 to 1.2 mg/dl [0.01 to 0.5 mmol/L], mean 0.8 mg/dl [0.33 mmol/L]) before and after correction with parenteral magnesium sulfate. Only three patients, all with hypocalcemia, had tremor and muscle twitching and none showed tetany, a positive Trousseau's test, arrhythmias, or ECG abnormalities. Moreover, review of the literature on hypomagnesemia did not justify attributing these clinical symptoms to hypomagnesemia. In a follow-up study of 111 consecutive serum samples from hypocalcemic patients, 36 (32%) indicated hypomagnesemia (serum Mg no greater than 1.5 mg/dl [0.6 mmol/L]); however, hypomagnesemia had been unsuspected in all but two patients. We conclude that hypomagnesemia rarely shows specific signs or symptoms; its diagnosis depends on a high index of suspicion in patients with hypokalemia, especially after its correction, and in patients with unexplained hypocalcemia.
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Abstract Magnesium plays an essential role in a wide range of fundamental biological reactions. Although diets consumed by healthy Americans usually do not lead to clinically significant magnesium depletion, epidemiological and clinical studies have suggested an association between low magnesium status and increased risk of cardiovascular diseases, hypertension, osteoporosis, diabetes, and other chronic diseases. In acutely or chronically ill hospitalized patients, the prevalence of hypomagnesemia has been reported to be as high as 11%. Hypomagnesemia resulting from underlying disease can be due to decreased gastrointestinal absorption or increased renal magnesium losses. Magnesium is principally an intracellular cation. Tissue magnesium status is difficult to accurately estimate with non‐invasive measures due to poor correlations between serum or RBC or WBC magnesium levels and magnesium concentration in major tissue stores in muscle and the skeleton. At present, a comprehensive evaluation of a patient's risk of magnesium deficiency should include consideration of known risk factors and disease conditions possibly contributing to magnesium depletion, estimates of dietary magnesium intake, and clinical observations. The evaluation also should include laboratory measures of magnesium status, including analysis of both extracellular (serum magnesium) and intracellular (RBC, WBC or muscle magnesium) magnesium concentration, if available. Researchers should continue efforts to find a simple, reliable, and useful technique to accurately estimate magnesium status.
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Introduction: Metabolic causes of neonatal seizures with good prognosis are hypoglycemia, hypocalcemia, hypomagnesemia. Some of hypocalcmic seizures are accompanied by hypomagnesemia, but magnesium levels are rarely investigated in resource restricted hospitals. Materials and Methods: A group of 150 neonates with seizures were studied. Analysis of serum Calcium, Magnesium and Sodium were done on the samples using conventional methods. Prevalence of hypomagnesemia, hypocalcemia and their association was estimated. Results: Metabolic abnormalities were present in 89 (59.3%) out of 150 cases. Of these, hypoglycemia and hypocalcemia were the most common with 39 (43.8%) and 28 (35.4%) cases respectively. The prevalence of hypomagnesemia was 5.3%. 87% of hypomagnesemia cases were associated with hypocalcemia implying the interrelation in pathophysiology. Among neonates with hypocalcemia, 20% had hypomagnesemia. Hence, there is a need to estimate magnesium levels in neonatal seizures because treatment is definitive with magnesium salts. Conclusion: Hypomagnesemia was a significant cause of neonatal seizures. Most of the neonates with hypomagnesemia had an associated hypocalcemia. It is necessary to estimate levels of magnesium in addition to calcium in all neonates with seizures.
Metabolic disorder
Magnesium deficiency (plants)
Neonatal hypoglycemia
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