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PubMed1987

Magnesium deficiency: pathogenesis, prevalence, and clinical implications.

Hypomagnesemia is probably the most underdiagnosed electrolyte deficiency in current medical practice. Patients with cardiovascular disease who are at greatest risk for the development of magnesium deficiency are those treated with diuretics or digitalis. Both potassium and magnesium deficiencies are associated with increased ventricular ectopy and may increase the risk of sudden unexpected death. Refractory potassium repletion can be caused by concomitant magnesium depletion, and can be corrected with magnesium supplementation. Routine serum magnesium determination is recommended whenever the testing of electrolyte levels is required, especially in patients taking diuretic drugs or digitalis. Because hypomagnesemia is not necessarily present in a magnesium-deficient state, it is recommended that both potassium and magnesium be repleted in patients with hypokalemia. Potassium-/magnesium-sparing diuretics may be helpful in the prevention of these electrolyte deficiencies.

Animals↗
PubMed1999

Magnesium deficiency and bone loss after cardiac transplantation.

Magnesium depletion adversely affects many phases of skeletal metabolism and has been implicated as a risk factor in several forms of osteoporosis. Magnesium deficiency has also been reported after cardiac transplantation. To evaluate whether altered magnesium homeostasis could be related to the pathogenesis of early bone loss after cardiac transplantation, we prospectively measured serum and urinary magnesium and evaluated them with respect to biochemical indices of mineral metabolism and rates of bone loss. The study population included 60 patients (45 men, 15 women) aged 53 +/- 11 years (SD) with measurements of biochemistries and bone mineral density by dual-energy X-ray absorptiometry before and 3 months after transplantation. All received prednisone, cyclosporine A, and azathioprine, plus calcium (1000 mg) and vitamin D (400 IU). After transplantation, serum magnesium decreased by 16 +/- 15% (SD) from 2. 0 +/- 0.3 mg/dl to 1.6 +/- 0.2 mg/dl (normal 1.8-2.2 mg/dl; p < 0. 0001), accompanied by an increase in the fractional excretion of magnesium (7.1 +/- 3.9% to 13.3 +/- 5.6%; p < 0.0017). Forty-three patients with low 3-month serum magnesium levels (</= 1.7 mg/dl) sustained 41% less bone loss at the lumbar spine (4.0 +/- 4.6% vs. 6. 8 +/- 5.3%; p = 0.051) and 58% less bone loss at the femoral neck (3. 1 +/- 5.9% vs. 7.3 +/- 5.6%; p < 0.01), despite receiving similar doses of prednisone and cyclosporine A. Of the biochemical parameters measured (including renal function, serum calcium, phosphorus, vitamin D metabolites, osteocalcin, urinary calcium, and markers of bone resorption), only intact parathyroid hormone (PTH) levels, which were 40% lower in patients with low serum magnesium levels differed significantly (45 +/- 23 pg/ml vs. 74 +/- 60 pg/ml; p = 0.019). Patients with low serum magnesium levels also had evidence of lower bone turnover. In summary, a highly significant decline in serum magnesium concentrations, associated with continued urinary magnesium losses, occurs after cardiac transplantation. Patients with low serum magnesium levels had significantly lower rates of bone loss, lower serum PTH concentrations, and lower bone turnover. Although the precise mechanisms by which the reduction in serum magnesium tends to protect against bone loss in the early post-transplantation period remain to be elucidated, reduced serum PTH and lower rates of bone turnover are likely to be important factors.

Adult↗
PubMed2004

Relationship between the degree of intracellular magnesium deficiency and the frequency of chest pain in women with variant angina.

OBJECTIVES: This study sought to clarify the relationship between the degree of intracellular magnesium deficiency and the frequency of anginal attacks in women with variant angina. PATIENTS AND METHODS: We evaluated the intracellular and extracellular magnesium status of twelve women with variant angina: group A (> or = 4 attacks/week, n = 5) and group B (< 4 attacks/week, n = 7). Magnesium levels were determined in serum, urine, and erythrocytes, and the 24-h magnesium retention rate was calculated by magnesium loading test. RESULTS: Group A showed a higher 24-h magnesium retention rate (58.2 +/- 9.1% vs. 31.3 +/- 4.4%; p < 0.01) and a lower intracellular concentration of magnesium in erythrocytes than group B (3.1 +/- 1.1 vs. 5.0 +/- 0.8 fg/cell; p < 0.05), demonstrating the presence of magnesium deficiency in group A. The 24-h magnesium retention rate and intracellular concentrations of magnesium in erythrocytes correlated well with the activity of variant angina (r = 0.61, p < 0.01; and r = -0.74, p < 0.01, respectively) for these patients. CONCLUSION: This study demonstrates that the degree of intracellular magnesium deficiency in women with variant angina is closely related to the frequency of chest pain.

Aged↗
PubMed1992

Magnesium-deficiency elevates circulating levels of inflammatory cytokines and endothelin.

We have developed two rodent models of diet-induced magnesium-deficiency in which histologically defined cardiac lesions can be induced within two to three weeks. During the development of these lesions, the magnesium-deficient animals exhibit circulating cytokine levels which are indicative of a generalized inflammatory state. Dramatic elevations of the macrophage-derived cytokines, IL-1, IL-6, and TNF-alpha together with significantly elevated levels of the endothelial cell-derived cytokine, endothelin, were detected in the plasma of these animals. We believe that the pathophysiological effects caused by the action of these cytokines may play a role in the promotion of cardiovascular pathology associated with magnesium deficiency.

Animals↗
PubMed1992

Magnesium deficiency: recognition and treatment in the emergency medicine setting.

Magnesium deficiency and its clinical manifestations are common in patients presenting to the emergency department. Assessment of the total body magnesium status of a patient is problematic since the serum magnesium concentration, the only readily available clinical test for this condition, may not be accurate in predicting the intracellular magnesium concentration. Therefore, empiric magnesium therapy should be considered in high-risk patients. Since magnesium participates in numerous metabolic processes in the body, a deficiency can affect multiple organ systems and present clinically in a variety of ways. Magnesium deficiency is reviewed in this paper with regard to therapeutic implications; specific treatment guidelines are given including dose, infusion rate, and magnesium preparation. Magnesium is also reviewed with regard to its homeostasis and metabolic role in the body. Special mention is made regarding precautions for use of magnesium in the setting of renal insufficiency.

Emergencies↗
PubMed2000

Magnesium deficiency potentiates free radical production associated with myocardial infarction.

OBJECTIVE: Oxidative injury and magnesium deficiency may accompany cardiovascular disease states and the study was planned to find out whether magnesium deficiency promotes oxidative injury. METHODS: Serum malonaldehyde (MDA), magnesium, vitamin E and total glutathione levels (GSH) were estimated in 22 patients with acute myocardial infarction and 15 healthy controls. RESULTS: Low levels of Mg, GSH, vitamin E and elevated levels of MDA were observed in patients of acute myocardial infarction. Statistically significant correlations were observed between Mg and MDA, MDA and GSH, Mg and vitamin E. CONCLUSION: Our findings suggest that Mg deficiency can potentiate oxidative injury to post ischaemic myocardium and that antioxidants may have a role in protection against the prooxidant influence(s) of Mg deficiency.

Aged↗
PubMed1981

Effect of magnesium deficiency and excess on renal tubular potassium transport in the rat.

1. Dietary magnesium deficiency is commonly associated with significant potassium depletion although the mechanisms responsible are unknown. Because the kidney has an important role in both magnesium and potassium homeostasis, clearance and micropuncture experiments were performed on thyroparathyroidectomized magnesium-deficient, normal and hypermagnesaemic rats to study the effect of body magnesium status on renal potassium handling. 2. Dietary magnesium restriction that reduced total-body magnesium by 30% did not alter renal potassium excretion despite a 10% reduction in total-body potassium. Graded magnesium infusions increased the fractional excretion of potassium in both magnesium-depleted and normal rats. However, the increase in the dietary depleted group was significantly less than in the control group (5-10 and then 13% compared with 7-19 and then 28% respectively). These changes in urine potassium excretion followed alterations in distal-tubule function. Parathyroid hormone did not alter potassium excretion in any of the experimental groups in contrast with its effect on magnesium excretion. 3. These data support the concept of distal tubular control of renal potassium homeostasis. The body magnesium status appears to exert some control over cellular potassium content and to alter indirectly distal-tubule potassium excretion.

Animals↗
PubMed1988

Magnesium deficiency in patients with ischemic heart disease with and without acute myocardial infarction uncovered by an intravenous loading test.

An intravenous magnesium-loading test with 30 mmol/L of magnesium was used to evaluate the magnesium status in 38 patients with ischemic heart disease (IHD) admitted to the coronary care unit with suspected acute myocardial infarction (AMI), in ten healthy volunteers (control group), and in nine patients with chronic IHD in a stable phase of their disease (chronic IHD group). Sixteen of the patients admitted with acute disease proved to have AMI (AMI group) and 22 did not (non-AMI group). Patients with IHD both with and without AMI retained significantly more magnesium (9.3 and 10.7 mmol/L [22.6 and 26 mg/dL], respectively) than did the control group (1.4 mmol/L [3.4 mg/dL]). This 34% magnesium retention points to a state of magnesium deficiency in patients with IHD. However, since the patients with and without AMI did not differ, the observations do not indicate that AMI is associated with a more severe magnesium deficiency than that found in other IHD patients without AMI. When the patients with IHD were subgrouped according to long-term diuretic treatment, the patients (n = 19) receiving long-term diuretic treatment had a 39% retention of magnesium (11.6 mmol/L [28.2 mg/dL]) compared with a 29% retention (8.7 mmol/L [21.1 mg/dL]) observed in 19 patients who were not receiving long-term diuretic treatment. This observation was not influenced by the presence or absence of AMI. An even higher level of magnesium retention (17.1 mmol/L [41.6 mg/dL] equals 57% retention) was found when investigating patients with chronic ischemic heart disease in a stable phase of their disease. This indicates that patients with IHD may be severely magnesium deficient; that long-term diuretic treatment contributes to this deficiency, but that diuretic treatment per se is not the only cause of this condition.

Aged↗
PubMed1998

Purification and characterization of 38-kDa protein in plasma of dietary magnesium-deficient rat.

We have found an increase of a 38-kDa plasma protein level from 10 to 30 days in rats on a magnesium-deficient diet (Mg; 0.001 per cent), using sodium dodecylsulfate-polyacrylamide gel electrophoresis (SDS-PAGE). This 38-kDa protein returned to the control level after feeding the rats a magnesium-sufficient diet (Mg; 0.07 per cent) for 1 week. Purification of the protein by reverse-phase HPLC separated it into two components (p38k-1 and p38k-2). Amino acid analysis showed that these components were both haptoglobin (Hp) beta-chain. Furthermore, hemoglobin-immobilized affinity chromatography analysis confirmed the increase of Hp in magnesium-deficient rat plasma. This is the first demonstration of an increase of Hp in plasma of dietary magnesium-deficient rats.

Amino Acid Sequence↗
PubMed1989

Mechanism of increased erythrocyte membrane fluidity during magnesium deficiency in weanling rats.

The erythrocyte membrane was investigated in weanling male rats pair fed with magnesium-deficient and control diets for 8 days. Fluorescence polarization studies revealed a 15% increase in the fluidity of membranes from deficient rats. A similar increase in the fluidity of liposomes indicated that protein was not involved. The change was associated with decreased osmotic fragility of intact erythrocytes; the cells lost their biconcavity and had a flattened appearance with surface irregularities. Analysis of the membranes showed decreased amounts of magnesium, cholesterol, and sphingomyelin in the deficient group. The reduced ratios of cholesterol to phospholipid and sphingomyelin to phosphatidylcholine were consistent with the increased fluidity. Addition of physiological amounts of magnesium to the medium rigidified membranes incubated in tris(hydroxymethyl)-aminomethane buffer, and this was prevented by the presence of EDTA. Cross-incubation experiments with erythrocyte ghosts and plasma from the two groups of rats showed that magnesium-deficient plasma increased the fluidity of control ghosts and control plasma rigidified ghosts from magnesium-deficient rats. Addition of sufficient magnesium chloride to raise the magnesium content of deficient plasma to normal had no significant effect. These results show that the increased fluidity of the erythrocyte membrane in magnesium deficiency is due to physicochemical exchange with the plasma. Although magnesium can directly influence membrane fluidity, the change during its deficiency in vivo is mainly mediated indirectly via disturbances in lipid metabolism.

Animals↗
PubMed1997

Magnesium deficiency and cardiogenic shock after cardiopulmonary bypass.

Magnesium is an important cation that has a key role in cellular processes of energy transfer and utilization involving adenosine triphosphate, and influences cell membrane functions. Its antiarrhythmic properties are well-known and it is widely recognized as an adjunct for the treatment of arrhythmias after myocardial infarction and cardiopulmonary bypass. Magnesium may influence hemodynamic performance through its effects on vascular tone, modulation of intracellular calcium, regulation of catecholamine activity, and its essential role in adenosine triphosphate metabolism. The potential for magnesium deficiency to affect cardiovascular performance may be especially relevant in ischemic states. We report a case of cardiogenic shock developing after cardiopulmonary bypass that was initially unresponsive to therapeutic intervention, but that resolved promptly after magnesium administration. The potential role of magnesium in enhancing hemodynamic performance is discussed, with a review of its cellular metabolic properties and activities.

Cardiopulmonary Bypass↗
PubMed1981

Changes in histamine and white blood cells in the blood, spleen and thymus of magnesium-deficient rat.

Groups of rats were given either a control or a magnesium-deficient diet. The well-known allergy-like crisis, characterized by vasodilatation with redness of the ears and dermatosis, occurred spontaneously in the magnesium-deficient groups. The histamine (H) content and the distribution of the various white blood cells (WBC) were studied as a function of time. During the acute phase, there was a transitory elevation of total blood H and WBC, mainly affecting the polymorphonuclear (PMN) cells, eosinophils (EO) and basophils (BAS). The EO peak preceded that of H. The EO count was especially high during the first part of the acute phase, while H and BAS were higher during the second part of that phase. There were no BAS's in the blood of the controls and those in the Mg-deficient animals were only partly granulated. H, EO and mast cells (MC) were elevated in the spleen but not in the thymus during acute deficiency. The high H level in the spleen corresponded to the same high level in the blood. When the spleen suspensions were centrifuged, wide differences in supernatant and pellet histamine appeared, according to the deficiency period.

Animals↗
PubMed1977

Effects of magnesium deficiency on protein and nucleic acid synthesis in vivo.

The effects of magnesium deficiency on the in vivo incorporation of labeled precursors into tissue macromolecules were studied. In severe Mg deficiency developing over 4 months, total protein synthesis in spleen and thymus was depressed by 40% to 50%, while DNA synthesis was increased by as much as 350%. RNA synthesis was not significantly altered. Protein synthesis in kidney was also reduced. In the intact liver, DNA synthesis was increased and RNA synthesis reduced, but protein synthesis was unchanged. The regeneration of the liver after partial hepatectomy was impaired, however, which suggested that the capacity of the liver protein synthetic system was reduced. The effects of magnesium deficiency were unaltered by the ingestion of ethanol that comprised approximately 25% of total energy. Each of the organs enlarged in Mg deficiency, and the spleen was strikingly hyperplastic. The increase in splenic DNA synthesis in the presence of depressed protein synthesis may be an early stage in a lymphoproliferative process leading ultimately to neoplasia.

Animals↗
PubMed1995

Dietary magnesium deficiency in rats enhances free radical production in skeletal muscle.

Recent studies suggest that free radicals may be involved in tissue injuries induced by magnesium deficiency. The aim of the present study was to assess the effect of magnesium deficiency on free radical production of skeletal muscle tissue. Male Wistar rats were pair-fed from weaning for 12 d either control or Mg-deficient diets containing 960 or 40 mg magnesium/kg diet, respectively. In the Mg-deficient rats, hypomagnesemia was accompanied by significantly lower magnesium and greater calcium concentrations in skeletal muscle tissue. Electron microscopy of skeletal muscle tissue revealed ultrastructural changes, including swelling mitochondria and disorganization of the sarcoplasmic reticulum network. Using the spin-trapping technique, we showed that significantly more hydroxyl radicals were generated in muscle homogenates of Mg-deficient rats. Moreover, the amount of spin trap adducts was increased in the presence of exogenous iron in both groups. In agreement with these observations, a greater concentration of thiobarbituric acid-reactive substances and a lower concentration of thiol groups were found in skeletal muscle of the Mg-deficient group compared with controls. These results strongly support the hypothesis that free radical-mediated injury could contribute to skeletal muscle lesions resulting from magnesium deficiency.

Animals↗
PubMed2001

A triple-risk model for the sudden infant death syndrome (SIDS) and the apparent life-threatening episode (ALTE): the stressed magnesium deficient weanling rat.

A triple risk model for the sudden infant death syndrome (SIDS) as described by Filiano and Kinney involves the intersection of three risks: (1) a vulnerable infant, (2) a critical developmental period in homeostatic control, and (3) an exogenous stressor(s). The triple risk model aptly describes the dynamics of an animal model for SIDS: (1) a vulnerable animal that is young and magnesium deficient: (2) a critical developmental period revealed by hyperirritability, labile cardiovascular and respiratory control; and (3) an exogenous stressor such as soft, high-pitched noise; motion or handling; or a chill. Together these three risks may trigger a shock-like episode of apnea, unconsciousness and bradycardia. The lung is the shock organ. An animal that dies quietly or after physical activity following the episode, models SIDS. However, if the shock-like episode resolves spontaneously or after resuscitation, the survivor is a model for an apparent life-threatening episode (ALTE). If, while still in the critical developmental period the ALTE survivor is stressed again, there is a risk for a recurrent episode, with the final outcome still unpredictable but with increasing risk for SIDS with multiple recurrences. The purpose of this communication is to present an illustrated review of the magnesium deficient weanling rat as an animal model for SIDS/ALTE, showing pertinent physical, electrocardiographic and pathological features. In the weanling rat, magnesium deficiency appears to be the single common pathway upon which multiple stressors may impinge to produce sudden death during the relatively brief critical developmental period, while magnesium supplements may protect the animal. If significant magnesium deficiency is subsequently diagnosed in a properly controlled study of human SIDS tissue, it is likely that a high proportion of SIDS deaths could be prevented by simple oral magnesium supplementation to infants during the first critical weeks and months of life.

Animals↗
PubMed2002

Synergistic effect of ofloxacin and magnesium deficiency on joint cartilage in immature rats.

Single high oral doses of fluoroquinolones (e.g., 1,200 mg of ofloxacin/kg of body weight) are chondrotoxic in juvenile rats. Characteristic cartilage lesions are detectable as early as 12 h after treatment. Since this dosing regimen does not reflect the therapeutic situation, we studied the effects of a 5- or 7-day treatment with ofloxacin at lower oral doses (10, 30, and 100 mg/kg twice a day [b.i.d.]) on joint cartilage in 4-week-old rats. We additionally investigated whether the effects of ofloxacin under these conditions are enhanced in animals kept on a magnesium-deficient diet during treatment. Knee joints were examined histologically. The concentrations of ofloxacin and magnesium were determined in plasma and cartilage. The lowest ofloxacin dose at which cartilage lesions occurred in animals on a standard diet was 100 mg/kg b.i.d. for 5 days. Peak plasma ofloxacin levels were approximately 10 mg/liter in these rats and thus were in the same range as the levels in the plasma of humans during therapy with high doses of ofloxacin. Treatment with 30 mg of ofloxacin/kg b.i.d. for 7 days caused no cartilage lesions in rats on a standard diet, but lesions did occur in 10 of 12 rats that were simultaneously fed a magnesium-deficient diet. Magnesium concentrations in bone, plasma, and cartilage from animals on an Mg(2+)-deficient diet were significantly lower than those in the controls. The concentration in plasma from animals on an Mg(2+)-deficient diet was 0.27 +/- 0.03 mmol/liter, whereas it was 0.88 +/- 0.08 mmol/liter in plasma from rats on a standard diet (means +/- standard deviations). Ofloxacin treatment did not change the total magnesium concentrations in tissues, as determined with ashed samples. The incidence of ofloxacin-induced lesions was higher in the magnesium-deficient animals, suggesting a synergistic effect. These results must be taken into account for a benefit-risk evaluation if ofloxacin is considered for use in the pediatric population.

Animals↗
PubMed1999

Effect of magnesium-deficient diet on serum and urine magnesium concentrations in healthy cats.

OBJECTIVE: To evaluate the efficacy of using serum total and ionized magnesium (Mg) concentrations and urine Mg concentrations to identify Mg deficiency in cats. ANIMALS: 6 healthy castrated male cats. PROCEDURE: A Mg-replete diet was fed for 37 days, followed by a Mg-deficient diet for 37 days. On days 1, 3, and 7 of the last week of each diet, serum ionized and total Mg concentrations were determined; in addition, urine Mg concentration was determined each day of the last week. Serum total and ionized Mg concentrations were compared with urine Mg concentration, amount of Mg excreted during 24 hours (24-hour urine Mg excretion), ratio of urine Mg concentration to urine creatinine concentration (Umg:Ucr), and urinary fractional excretion of Mg (FEmg) to determine which variable best predicted Mg status. RESULTS: Cats fed Mg-deficient diets had significantly lower serum total and ionized Mg concentrations and 24-hour urine Mg excretion values, compared with cats fed Mg-replete diets. Serum total Mg concentration was the best predictor of Mg status. Twenty-four-hour urine Mg excretion was a repeatable, reliable measurement and had the best correlation with serum total Mg concentration. Serum total Mg concentration also correlated with urine Mg concentration, Umg:Ucr, and FEmg. CONCLUSIONS AND CLINICAL RELEVANCE: Serum total and ionized Mg concentrations can be used to identify cats with dietary-induced Mg deficiencies. Twenty-four-hour urine Mg excretion and urine Mg concentration correlated best with serum total Mg concentration and, therefore, may be the most useful urine variables for identifying Mg deficiency.

Animal Feed↗
PubMed1987

Magnesium deficiency produces endothelium-dependent vasorelaxation in canine coronary arteries.

In the present study, effects of magnesium deficiency on coronary vascular reactivity changes were studied in isolated canine coronary arteries before and after endothelium disruption. Lowering of extracellular magnesium produced a potent vasorelaxant response in coronary arteries with intact endothelium, whereas in arteries with disrupted endothelium a potent vasoconstrictory response was observed. The magnitude of magnesium deficiency-induced vasorelaxation is also dependent on the extracellular calcium concentrations, such that lowering of extracellular calcium from 1.75 to 0.22 mM completely abolished the magnesium deficiency-induced vasorelaxant effects. Similar inhibition, as well as reversal, of magnesium deficiency-induced vasorelaxation was also observed with dichlorobenzamil, a known inhibitor of the Na+/Ca++ exchange mechanism, but not with nifedipine, a known inhibitor of the voltage-operated calcium channel. The magnesium deficiency-induced vasoconstriction, on the other hand, is endothelium-independent. Although a similar dependency on extracellular calcium concentration was observed in this vasoconstrictory response, nifedipine, but not dichlorobenzamil, was found to be effective in inhibiting the vasoconstrictory effect. Hemoglobin, a known inhibitor of the endothelium-derived relaxing factor, also completely inhibited the magnesium deficiency-induced vasorelaxation but had no effect on the latter vasoconstrictory effect. These results suggest that circulating magnesium ion may have a dual effect in the modulation of coronary vascular reactivity. In coronary vessels with intact endothelium, lowering of extracellular magnesium may potentiate calcium-induced basal release of endothelium-derived relaxing factor and result in vasodilation, whereas in pathological vessels with injured endothelial cells, a similar lowering of magnesium may increase coronary vascular tone by accentuating the calcium-induced coronary constrictory response in vascular smooth muscle cells and result in vasoconstriction.

Amiloride↗