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PubMed1976

Functional hypoparathyroidism and parathyroid hormone end-organ resistance in human magnesium deficiency.

Hypocalcaemia is a well-recognized manifestation of magnesium deficiency. We have studied seventeen patients with this syndrome in an attempt to determine the pathogenesis of the hypocalcaemia. Mean initial serum calcium concentration was 5-6 mg/dl and mean initial serum magnesium concentration was 0-75 mg/dl. Serum immunoreactive parathyroid hormone (IPTH) was measured in sixteen patients in the untreated state. Despite severe hypocalcaemia, serum IPTH was either undetectable (less than 150 pg/ml) or normal (less than 550 pg/ml) in all but two patients. Serial measurements made during the initial 4 days of magnesium therapy in four patients showed an increase in serum IPTH within 24h, but a delayed increase in serum calcium, which required approximately 4 days to reach normal values. The effect of the rapid normalization of serum magnesium on serum IPTH and serum calcium concentration was studied in three patients. Within 1 min after 144-300 mg of elemental magnesium was administered i.v., serum IPTH had risen from undetectable to 3600 pg/ml and 1725 pg/ml in two patients and from 425 pg/ml to 937 pg/ml in the third. Serum calcium concentrations were unchanged after 30-60 min. These data provide evidence for impaired parathyroid gland function in most of the magnesium deficient patients. The rapidity with which serum IPTH rose in response to magnesium therapy indicates that this may reflect a defect in parathyroid hormone (PTH) secretion rather than its biosynthesis. The failure of serum calcium concentration to increase during the initial days of magnesium repletion, at a time when serum IPTH concentrations were normal or elevated, suggests end-organ resistance to PTH in these patients. The renal response to PTH was examined in two magnesium deficient patients by measurement of urinary cyclic AMP excretion following administration of parathyroid extract. In both patients there was a minimal increase in urinary cyclic AMP concentrations. In contrast, when the hepatic response to glucagon was tested on the same patients by measurement of plasma cyclic AMP concentrations following administration of glucagon, normal increases were observed. These results suggest that adenylate cyclase systems of various organs may be affected differentially by a state of magnesium deficiency. It is suggested that magnesium deficiency may result in defective cyclic AMP generation in the parathyroid glands and in the PTH target organs. This could be the principal mechanism operative in both impaired PTH secretion and end-organ resistance to PTH which together contribute to the development of hypocalcaemia.

Adult↗
PubMed1984

Magnesium deficiency in the Japanese quail.

Morphological effects of magnesium deficiency on liver cells and general aspects of its influence on the metabolism were investigated in young quails. Magnesium deficiency was characterized by a depressed growth, a high mortality rate, a decrease in hematocrit and magnesium and calcium plasma concentrations. Magnesium deficiency reduced the magnesium concentration in heart by 44%, but did not affect the concentration in liver. Ultrastructural aspect of liver parenchymal cells revealed that the number of mitochondria per cell section was decreased and the average area of a mitochondrion was greater in deficient quails than in control animals. The significance of these morphological changes was discussed in relation to disturbances in energy metabolism of these organelles. From these results, japanese quail appeared as an interesting experimental model for studies on metabolic disturbances in magnesium deficiency.

Animals↗
PubMed1993

Oxalate metabolism in magnesium-deficient rats.

Male weanling rats were maintained on magnesium-deficient diet for 30 d and compared with pair-fed control rats fed magnesium-supplemented diet. Magnesium deficiency led to slow growth and finally to a significant decrease in body weight (P < 0.001) accompanied by a significant hypomagnesaemia, hypomagnesuria and hyperoxaluria (P < 0.001 in each case) in experimental rats as compared to the control rats. Magnesium deficiency altered the glyoxylate metabolism in the liver and kidney mitochondria by significantly decreasing glyoxylate oxidation (by 26 per cent in liver and 17 per cent in kidney) and activity of alpha-ketoglutarate:glyoxylate carboligase enzyme (by 35 per cent in liver and 27 per cent in kidney) in the experimental animals. A significant increase in the specific activities of glycolic acid oxidase (P < 0.001) and glycolic acid dehydrogenase (P < 0.01) and a significant decrease in alanine transaminase (P < 0.01) was also observed in magnesium-deficient rats. No change in liver and kidney lactate dehydrogenase was observed. Thus magnesium deficiency in rats leads to accumulation of glyoxylate in the tissues, a part of which is converted into oxalate, thereby promoting hyperoxaluria.

Aldehyde-Ketone Transferases↗
PubMed2006

Cardiac fibrogenesis in magnesium deficiency: a role for circulating angiotensin II and aldosterone.

Mechanisms underlying cardiac fibrogenesis in magnesium deficiency are unclear. It was reported earlier from this laboratory that serum from magnesium-deficient rats has a more pronounced stimulatory effect on cell proliferation, net collagen production, and superoxide generation in adult rat cardiac fibroblasts than serum from rats on the control diet. The profibrotic serum factors were, however, not identified. This study tested the hypothesis that circulating angiotensin II may modulate cardiac fibroblast activity in hypomagnesemic rats. Male Sprague-Dawley rats were pair-fed a magnesium-deficient (0.0008% Mg) or -sufficient (0.05%) diet for 6 days, and the effects of serum from these rats on [3H]thymidine and [3H]proline incorporation into cardiac fibroblasts from young adult rats were evaluated in the presence of losartan, an angiotensin II type 1 (AT1) receptor antagonist, and spironolactone, an aldosterone antagonist. Losartan and spironolactone markedly attenuated the stimulatory effects in vitro of serum from the magnesium-deficient and control groups, but the inhibitory effects were considerably higher in cells exposed to serum from magnesium-deficient animals. Circulating and cardiac tissue levels of angiotensin II were significantly elevated in magnesium-deficient animals (67.6% and 93.1%, respectively, vs. control). Plasma renin activity was 61.9% higher in magnesium-deficient rats, but serum angiotensin-converting enzyme activity was comparable in the two groups. Furthermore, preliminary experiments in vivo using enalapril supported a role for angiotensin II in magnesium deficiency. There was no significant difference between the groups in serum aldosterone levels. The findings suggest that circulating angiotensin II and aldosterone may stimulate fibroblast activity and contribute to a fibrogenic response in the heart in magnesium deficiency.

Aldosterone↗
PubMed1996

Environmental magnesium deficiency as a cardiovascular risk factor.

Magnesium is abundant in nature and the major routes of intake are through food and water. Through changes in the treatment of foodstuffs and altered diets, as well as increased use of surface water with low magnesium content, magnesium deficiency is present in modern society. Magnesium deficiency causes cardiac arrhythmia and several studies suggest that a low level of magnesium in drinking water is a risk factor for myocardial infarction, particularly among men. Before general prevention programmes can be recommended, risk groups must be defined and experimental intervention programmes performed.

Cardiovascular Diseases↗
PubMed2000

Physiopathology of symptomatic and latent forms of central nervous hyperexcitability due to magnesium deficiency: a current general scheme.

Symptomatic forms of central nervous hyperexcitability (NHE) due to magnesium deficiency results from the sum of direct cellular effects and of local and systemic mediated effects inducing depolarization and NHE. Direct effects associate decreased energy and cationic gradient with disturbances in Ca distribution, decreased second messenger nucleotidic ratio and increased susceptibility to peroxidation. Local mediated effects associate increased activity of excitatory neuromediators: acetylcholine, catecholamines and ionotropic - (NMDA and non-NMDA) - receptors of excitatory aminoacids (EAA), with decreased activity of inhibitory neuromediators: GABA, taurine, glutaurine, adenosine and K receptors of opioids. Systemic mediated effects associate increased production of inflammatory mediators: neuropeptides, prostanoids, cytokines Th 1, aldehydes with decreased activity of oxidant and antialdehyde defences. Compensatory factors instrumental in the latency of NHE due to magnesium deficiency may also be direct or mediated. Increased intracellular pH, modifications of Ca and Mg binding proteins, increase in 'magnesium-like' polyamines, stimulation of cellular antioxidant system; decreased activity of EAA metabotropic receptors and of opioid mu (and delta) receptors, increased activity of inhibitory neuromediators, increased production of anti-inflammatory mediator such as cytokines Th 2, stimulation of systemic antioxidant and antialdehyde defences. A lot of diverse compounds are able to palliate symptomatic NHE due to magnesium deficiency either by pharmacodynamic effects or through physiopathological intervention. The efficiency of these treatments can be evaluated on multiple disparate parameters. The pattern of NHE due to magnesium deficiency differs according to species, strains, gender, age and intensity of magnesium deficiency. For example: hot plate test showed a hypoalgesia 'morphine-like' pattern induced by magnesium deficiency cured by magnesium acetyltaurinate in mice whilst paw pressure test showed a hyperalgic pattern caused by magnesium deficiency cured by dizolcipine in rats. Now it seems difficult to rank hierarchically the various physiopathological mechanisms of NHE due to magnesium deficiency. But the proposed general scheme of the factors controlling this NHE provides a possible explanation of both diffuse symptomatic and latent forms and stresses the complexity of the physiopathological mechanisms of central NHE due to magnesium deficiency.

Animals↗
PubMed1985

Magnesium deficiency in the rat increases tissue levels of docosahexaenoic acid.

The effects of magnesium deficiency on tissue levels of total lipids and fatty acids were evaluated. Sprague-Dawley rats were fed a magnesium-deficient diet for 14 wk with controls being pair-fed to the deficient rats. Compared to the controls, serum and 24-h urinary magnesium levels were markedly lower in the magnesium-deficient rats. Serum cholesterol and total phospholipids were significantly higher in the magnesium-deficient rats than in the controls. Edema and polycystic degeneration of the kidneys were present in the magnesium-deficient rats. Kidney total phospholipids and triacylglycerols were significantly lower in the magnesium-deficient rats than in the controls. The main change in tissue fatty acid composition in magnesium deficiency was the higher docosahexaenoic acid (22:6n-3) in serum, liver and aorta than in controls. The possible relationship of these findings to human alcoholism is discussed.

Animals↗
PubMed1992

Magnesium deficiency diagnosed by an intravenous loading test.

Magnesium deficiency is common but difficult to diagnose and to assess in clinical practice. The use of a magnesium loading test was therefore evaluated to diagnose magnesium deficiency in 661 hospitalized patients with medical conditions assumed to interfere with magnesium uptake and excretion. Thirty millimoles of magnesium sulphate were administered intravenously during 8 h as a loading test and related to the urinary excretion in the following 24 h. A group of 30 patients without any known predisposition for magnesium deficiency and a group of 27 healthy volunteers served as controls. The mean (with 95% confidence interval) magnesium retention was 4 (-2-10)% in the control group of patients and 3 (-2-8)% in healthy subjects. A significantly higher retention was observed in all the groups of the patients: atrial fibrillation 18 (11-25)%, other arrhythmias 18 (11-24)%, hypertension 27 (20-33)%, coronary artery disease 25 (20-30)%, congestive heart failure 31 (26-37)%, cerebrovascular events 38 (24-51)%, gastrointestinal disorders 22 (14-29)%, diabetes mellitus 16 (9-22)%, and alcoholics 33 (29-36)%. The percentage of patients with a retention greater than mean + 2 SD of the two control groups varied between 22% and 54% among the different patient groups. The mean serum magnesium among the patient groups was similar to the control group of patients, except for the alcoholics, hypertensives and young healthy controls, who had significantly reduced levels. Magnesium retention was significantly correlated to age and renal function, and among the alcoholics negatively correlated to serum magnesium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

A magnesium load test in the diagnosis of magnesium deficiency.

The concentration of magnesium in muscle was determined and a standardized magnesium load test was performed in 21 patients, who 4 to 10 years previously had undergone intestinal bypass operations for severe obesity. The plasma concentration and 24-h urinary excretion of magnesium were also studied. Basic urinary excretion of magnesium and muscle magnesium were significantly lower in patients compared to healthy controls, while no differences were found in plasma magnesium. A slight negative correlation between muscle magnesium and retained magnesium was demonstrated (r = -0.51, P less than 0.05). Patients with magnesium retention greater than 20 per cent showed a significant decrease of magnesium retention after treatment with magnesium chloride mixture. Four patients with primarily low muscle magnesium all demonstrated an increment in the amount of magnesium in muscle after treatment. The load test described can be applied as a screening test in diagnosing magnesium deficiency.

Adult↗
PubMed1990

Effect of magnesium deficiency on lipid metabolism in uremic rats.

The effects of acute magnesium deficiency on lipid metabolism were examined in five-sixths nephrectomized uremic rats and sham-operated rats. Three weeks after the surgery, both groups were divided into two subgroups. Half of the uremic and sham-operated rats received a magnesium-deficient diet. The rest of the experimental animals received a control diet. After 2 weeks on this regimen, all animals were sacrificed. In uremic rats, magnesium deficiency increased serum triglyceride levels and decreased high-density lipoprotein cholesterol levels as in sham-operated rats. Total serum cholesterol levels were higher in uremic rats than in sham-operated rats with or without magnesium deficiency. Serum free fatty acid levels were increased only in uremic rats with magnesium deficiency. These results suggest that magnesium deficiency worsens several parameters of lipid in uremic rats.

Animals↗
PubMed2000

[Diagnosing magnesium deficiency. Current recommendations of the Society for Magnesium Research].

The cardiovascular risk increases with decreasing serum levels of magnesium, and this already at concentrations within the previous reference range (0.70-1.10 mmol/L). For this reason, the Society for Magnesium Research has updated its 1986 recommendations for the diagnosis of magnesium deficiency. The diagnosis is based on the patient's history, his clinical symptoms, and the results of clinical-chemical investigations of plasma/serum and urine. Further diagnostic methods used include the determination of ionized serum magnesium and the magnesium retention test. The optimal serum magnesium concentration is > 0.80 mmol/L.

Adolescent↗
PubMed2004

[Diagnosis of magnesium deficiency in the body, personal experience].

Magnesium as a component of a range of enzymatic systems is a very important intracellular cation in the organism. Its monitoring is limited in many observations only to determination of its concentration in blood serum. We have done an analysis of serum and erythrocyte magnesium concentrations in 23 healthy women, 70 healthy men and in 184 patients with ulcerative disease of gastroduodenum. It was proved in all the monitored groups that erythrocyte concentrations of magnesium were lower compared to values which were estimated from serum concentrations in 9 from 23 healthy women, in 3 from 60 healthy men, in 10 from 101 ill men with ulcerative gastroduodenal disease, and in 17 from 83 women with ulcerative gastroduodenal disease. The highest rate of low concentrations of erythrocyte magnesium in healthy women with physiologic concentrations of magnesium in serum was also confirmed by currently created subgroup of healthy women (n = 11) who undergone together with other analysis peroral Mg2+ load test. This test confirmed magnesium deficiency in 10 from 11 women. The results showed there are more frequent deficiencies of magnesium in organisms then it is generally assumed. They also proved the importance of nutrition and regular food in population of healthy, young women.

Adult↗
PubMed2004

Bone specific binding sites for 1,25(OH)2D3 in magnesium deficiency.

It has been reported that some hypoparathyroid patients with magnesium deficiency showed altered responses to vitamin D treatment. In the same way, in vitro bone studies have demonstrated the existence of a decrease in the 1,25-dihydroxyvitamin D3-induced resorption in bone as a result of magnesium deficiency. These findings suggest some kind of alteration in the 1,25(OH)2D3 in bone in magnesium deficiency. In the present work, using a binding assay based on the 1,25(OH)2D3 and 3H-1,25(OH)2D3 competition for the hormone binding sites in rat calvaria homogenates, a significant decrease in the number of 1,25(OH)2D3 specific binding sites has been found in calvaria incubated in magnesium-deficient medium compared to magnesium-replete ones. Alterations in the hormone-receptor affinity were not found. These results suggest that an alteration in the 1,25(OH)2D3 action on magnesium-deficient bone could be due, at least in part, to a decrease in the number of available vitamin D receptors in bone cells.

Animals↗
PubMed1975

Magnesium deficiency and cardiac disorders.

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.

Alcoholism↗
PubMed2005

The possible relationship between keratoconus and magnesium deficiency.

The cause of keratoconus is unknown. However, an earlier report demonstrated magnesium deficiency in keratoconus patients, and suggested that magnesium deficiency could pathologically affect the mechanisms of the cornea. Experimental and clinical papers concerning a possible relationship between keratoconus and magnesium deficiency were reviewed. These studies have demonstrated molecular and cellular alterations specific to the keratoconic cornea, including: thinning and fragmentation of membranes, degenerated cells and collagen fibres, swelling of the mitochondria, and biochemical abnormalities in protein synthesis. Similar alterations have reportedly been induced by magnesium deficiency. This review suggests a possible relationship between the specific keratoconic disorders and the alteration induced by magnesium deficiency at the intracellular and extracellular levels. Although the etiology of keratoconus is still unknown, this paper may give some new ideas for further experimental and clinical studies on the etiology of keratoconus.

Apoptosis↗
PubMed2001

Acute cytoskeletal alterations and cell death induced by experimental brain injury are attenuated by magnesium treatment and exacerbated by magnesium deficiency.

Traumatic brain injury results in a profound decline in intracellular magnesium ion levels that may jeopardize critical cellular functions. We examined the consequences of preinjury magnesium deficiency and post-traumatic magnesium treatment on injury-induced cytoskeletal damage and cell death at 24 h after injury. Adult male rats were fed either a normal (n = 24) or magnesium-deficient diet (n = 16) for 2 wk prior to anesthesia and lateral fluid percussion brain injury (n = 31) or sham injury (n = 9). Normally fed animals were then randomized to receive magnesium chloride (125 micromol, i.v., n = 10) or vehicle solution (n = 11) at 10 min postinjury. Magnesium treatment reduced cortical cell loss (p < 0.05), cortical alterations in microtubule-associated protein-2 (MAP-2) (p < 0.05), and both cortical and hippocampal calpain-mediated spectrin breakdown (p < 0.05 for each region) when compared to vehicle treatment. Conversely, magnesium deficiency prior to brain injury led to a greater area of cortical cell loss (p < 0.05 compared to vehicle treatment). Moreover, brain injury to magnesium-deficient rats resulted in cytoskeletal alterations within the cortex and hippocampus that were not observed in vehicle- or magnesium-treated animals. These data suggest that cortical cell death and cytoskeletal disruptions in cortical and hippocampal neurons may be sensitive to magnesium status after experimental brain injury, and may be mediated in part through modulation of calpains.

Animals↗
PubMed1988

Magnesium deficiency alters aggressive behavior and catecholamine function.

Magnesium is an abundant mineral in the brain and is important for monoamine neurotransmitter synthesis and receptor binding. It should, therefore, have behavior-altering effects. Three experiments were conducted to determine the influence of magnesium deficiencies on aggressive behavior and catecholamine function in mice. There were concentration- and time-dependent reductions in offensive aggressive behavior with magnesium deficiencies. Defensive behavior was affected in a manner opposite to that of offensive behavior. Upon administration of low doses of apomorphine and l-amphetamine, less dopamine- and norepinephrine-related behavior occurred with less magnesium in the diet. These reductions also showed a time dependency. These data demonstrate that magnesium has an influence on aggressive behavior in mice. Also, a magnesium deficiency is capable of altering the potency of catecholamine stimulating drugs.

Aggression↗
PubMed1998

Effects of fluoroquinolones and magnesium deficiency in murine limb bud cultures.

Quinolone-induced arthropathy is probably caused by a lack of functionally available magnesium in immature joint cartilage. We used an in vitro assay to study the effects of fluoroquinolones on cartilage formation in mouse limb buds from 12-day-old mouse embryos in regular and in magnesium-deficient medium. Omission of magnesium from the medium had no adverse effect on the outcome of the culture: limb buds grew and differentiated well in regular and in magnesium-deficient Bigger's medium. Lack of calcium, however, severely impaired the development of the explants; this result was even more enhanced when both minerals (magnesium and calcium) were omitted. Electron microscopy revealed cell necrosis and deposition of electron-dense material in the vicinity of chondrocytes from limb buds after 6 days in a magnesium-free medium. A series of seven fluoroquinolones was tested at 30, 60, and 100 mg/l medium. At a concentration of 30 mg/l sparfloxacin only had a slight effect on limb development. At concentrations of 60 and 100 mg/l sparfloxacin, temafloxacin and ciprofloxacin impaired limb development in vitro concentration-dependently. The effects were enhanced in a magnesium-deficient medium (concentration of magnesium <10 micromol/l). Fleroxacin, lomefloxacin and ofloxacin impaired limb development only slightly; no significant differences were recognizable between the outcome in regular and in magnesium-deficient medium. Pefloxacin did not show any effect on limb development in both media. Using electron microscopy, very similar alterations as described above for the limbs cultured in magnesium-deficient medium were observed with ofloxacin at a concentration of 30 mg/l, which had no effect on the growth of the explants when evaluated macroscopically. The affinity of six fluoroquinolones to magnesium was determined by the use of a fluorescence assay. The affinity to magnesium correlated with the activity of the drugs in the limb bud assay. We conclude that fluoroquinolones have no effect on murine limb development in vitro at concentrations that are achieved under therapeutic conditions (peak concentrations approx. 1-5 mg/l in plasma). Effects at higher concentrations (60 and 100 mg/l) are slightly enhanced (factor 2) if the magnesium concentration in the medium is low. Macroscopically, limbs develop regularly in a magnesium-free medium, but ultrastructurally typical alterations are exhibited (e.g. cell necrosis and pericellular deposition of electron-dense material).

Animals↗