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PubMed1984

Magnesium deficiency. Causes and clinical implications.

The many causes of clinical magnesium deficiency can be placed into 2 categories: diminished intake of magnesium, and enhanced losses of magnesium, either through the gastrointestinal tract or through the kidneys. Examples of the first category include alcoholism, starvation, anorexia due to neoplastic disease and/or chemotherapy. Examples of the second category include severe diarrhoeal states, gastrointestinal fistulae, malabsorption, diuretic therapy and gentamicin therapy. Estimates of the prevalence of clinical hypomagnesaemia range from 6 to 11% in hospitalised patients. Serum predictors of associated clinical magnesium depletion include hypokalaemia (42%), hyponatraemia (23%), hypophosphataemia (22%) and hypocalcaemia (20%). Experimental and clinical observations strongly support the view that magnesium and potassium are closely linked at the cellular level. Magnesium has been demonstrated to be important in cell energetics (Mg++-activated ATPase), in maintenance of the integrity of cell membranes, retardation of cell loss of potassium, as well as enhancing repletion of cell potassium. While translation of these experimental observations into clinical terms encompasses a wide spectrum of illnesses, there is special relevance in considering the role of magnesium in repletion and maintenance of cell potassium in 2 clinical instances: (a) patients treated with digitalis and diuretics; and (b) hypertensive patients. In these types of patients not only potassium but also magnesium should be administered together to avoid the problem of cell potassium depletion and refractory potassium repletion associated with coexisting and uncorrected magnesium depletion.

Digitalis Glycosides↗
PubMed2000

Magnesium deficiency and other risk factors for diabetic retinopathy.

A case control study was carried out to detect the relation between magnesium deficiency and diabetic retinopathy and to study other risk factors for diabetic retinopathy. The study involved 30 cases with diabetic retinopathy, 30 diabetics and 30 non-diabetics with normal retina as controls. Serum magnesium was significantly lower in the diabetic control group than both other groups. Significant association between diabetic retinopathy and hypertension, poor control of blood sugar, irregularity in drug treatment, lack of routine fundus examination, high gravidity and low socioeconomic status were found. Multiple regression analysis was used to adjust for all variables mentioned. Magnesium deficiency was found to be statistically significantly associated with diabetic retinopathy after considering the effects of other variables.

Diabetic Retinopathy↗
PubMed2000

Cisplatin ototoxicity, increased DPOAE amplitudes, and magnesium deficiency. Distortion product otoacoustic emissions.

Outer hair cell (OHC) metabolism is blocked by cisplatin. Concurrent changes in the renal handling of magnesium occur because of the damage cisplatin causes to the renal proximal tubule cells within the thick ascending loop of Henle. Although there is no evidence of cisplatin within the OHCs, there are significant levels of intracellular calcium, the antagonist to magnesium at the cell membrane. The OHC motile response is dependent on intracellular calcium. When the calcium current is suppressed by an antagonist, the extracellular OHC microphonic potential decreases. Magnesium deficiency is known to produce hyperexcitability within the central nervous system, including fatal audiogenic seizures. In addition, increases in the amplitude of the auditory brainstem response wave V occur with aminoglycoside therapy and magnesium deficiency. This paper illustrates the amplitude growth of distortion product otoacoustic emissions in two patients treated with cisplatin and explores the possible underlying reasons why this may be related to magnesium metabolism.

Adenocarcinoma↗
PubMed1998

Exacerbated immune stress response during experimental magnesium deficiency results from abnormal cell calcium homeostasis.

The aim of this study was to assess the potential mechanism underlying the enhanced inflammatory processes during magnesium deficit. In this study, exacerbated response to live bacteria and platelet activating factors was shown in rats fed a magnesium-deficient diet. Peritoneal cells from these animals also showed enhanced superoxide anion production and calcium mobilising potency following in vitro stimulation. The latter effect occurred very early in the course of magnesium deficiency. These studies first showed that an abnormal calcium handling induced by extracellular magnesium depression in vivo may be at the origin of exacerbated inflammatory response.

Animals↗
PubMedDate not supplied

Parasomnias (non-epileptic nocturnal episodic manifestations) in patients with magnesium deficiency.

Twenty seven patients with parasomnias (night terrors, nocturnal motor automatisms, nocturnal verbal automatisms and sometimes with bruxisms) associated with magnesium deficiency were selected. In all of them marked hypomagnesemia, clinical, EEG and EMG signs of spasmophilic syndromes were found. The 8 hours polysomnographical recordings of all cases (monitored in a system with infra-red video-TV cameras) showed severe sleep disorders and EEG nocturnal abnormalities occurring in the SWS (especially in the I b, II and III stages) with disappearance in the REM sleep. The authors suggest that these clinical and polysomnographic anomalies may be the expression of the brain damage caused by magnesium deficiency or of the clinical electrographic manifestations of the reticulate neuronal hypersynchrony exacerbated by sleep.

Adolescent↗
PubMed1986

Magnesium deficiency inhibits biosynthesis of blood glutathione and tumor growth in the rat.

Previously we found that blood glutathione (GSH) levels increase in response to tumor growth in the rat and that this increase is not prevented with zinc deficiency. We also found that zinc deficiency which inhibited tumor growth did not prevent this increase in blood GSH. Therefore, the objectives of this study were to determine the effects of another nutritional modification, namely magnesium deficiency, on blood GSH status and on tumor growth. Magnesium was selected because it is an obligatory cofactor in GSH synthesis and in all biosynthetic reactions involving ATP. To this end, magnesium- and zinc-deficient rats with and without tumors were compared to pair-fed control rats with and without tumors. After 32 days of depletion, the rats were killed, and blood samples were analyzed for nonprotein sulfhydryls (SH) and specifically for GSH. The key finding was that in magnesium-deficient rats with or without tumors, blood GSH levels were low and SH levels were normal indicating a decrease in GSH biosynthesis. In contrast, zinc deficiency affected SH and GSH in parallel. Thus, these two deficiencies must act by different mechanisms. The zinc data verified our earlier results obtained with a different tumor type and rat strain, for blood GSH levels increased in tumor-bearing rats fed control diets, and zinc deficiency did not prevent this increase. Depletion of magnesium or zinc was equally effective in inhibiting tumor growth. These results provide in vivo evidence of a magnesium requirement for GSH biosynthesis in rat erythrocytes. Further, the results suggest that magnesium deficiency may inhibit tumor growth by limiting GSH synthesis from SH precursors.

Animals↗
PubMed1991

Dietary fructose produces greater nephrocalcinosis in female than in male magnesium-deficient rats.

The synergistic interaction of fructose and magnesium (Mg) deficiency on kidney calcification was compared in male and female rats. Male and female weanling rats were divided into four dietary groups: fructose or starch, with or without Mg. Rats were fed their respective diets for 9 weeks, and 24 h urine was collected to measure urinary output, pH, Mg, calcium (Ca), and oxalic acid. Rats were fasted overnight. After decapitation, blood was collected immediately, and kidneys were removed to determine their Mg and Ca content. Dietary fructose significantly increased kidney Ca in female rats fed deficient or adequate Mg diet and in male rats fed Mg-deficient diet only; the greatest kidney calcification occurred in female rats fed Mg-deficient diet (P less than 0.0001). Even in starch groups female rats fed the Mg-deficient diet showed some kidney Ca accumulation. The synergistic interaction of fructose and magnesium deficiency on nephrocalcinosis was significantly greater in female than in male rats. Low urinary output, optimal pH 6.8 for calcium phosphate precipitation, hypercalcaemia, hypercalciuria, hypomagnesuria, and low ratio of urinary Mg to Ca may independently or multifactorially contribute to nephrocalcinosis. The possible mechanism of this interaction is discussed.

Analysis of Variance↗
PubMed1997

Effect of acute magnesium deficiency (MgD) on aortic endothelial cell (EC) oxidant production.

Magnesium deficiency (MgD) has been associated with production of reactive oxygen species, cytokines, and eicosanoids, as well as vascular compromise in vivo. Although MgD-induced inflammatory change occurs during "chronic" MgD in vivo, acute MgD may also affect the vasculature and consequently, predispose endothelial cells (EC) to perturbations associated with chronic MgD. As oxyradical production is a significant component of chronic MgD, we examined the effect of acute MgD on EC oxidant production in vitro. In addition we determined EC; pH, mitochondrial function, lysosomal integrity and general cellular antioxidant capacity. Decreasing Mg2+ (< or = 250microM) significantlyincreased EC oxidant production relative to control Mg2+ (1000microM). MgD-induced oxidant production, occurring within 30min, was attenuated by EC treatment with oxyradical scavengers and inhibitors of eicosanoid biosynthesis. Coincident with increased oxidant production were reductions in intracellular glutathione (GSH) and corresponding EC alkalinization. These data suggest that acute MgD is sufficient for induction of EC oxidant production, the extent of which may determine, at least in part, the extent of EC dysfunction/injury associated with chronic MgD.

Acute Disease↗
PubMedDate not supplied

Magnesium deficiency and diabetes mellitus.

Hypomagnesemia is the commonest electrolyte abnormality in the ambulatory diabetic patient and is also a frequent finding in patients with diabetic ketoacidosis. Excessive urinary magnesium loss associated with glycosuria is probably the most important factor in the genesis of hypomagnesemia in the diabetic patient. The clinical consequences of magnesium deficiency include impairment of insulin secretion, insulin resistance and increased macrovascular risk. The role of magnesium deficiency in microvascular complications has yet to be clearly defined.

Diabetes Mellitus↗
PubMed1991

Magnesium deficiency may be an important determinant of ventricular ectopy in digitalised patients with chronic atrial fibrillation.

Digitalised patients with chronic atrial fibrillation (AF) have a high prevalence of ventricular premature beats (VPB); magnesium deficiency may be a contributory factor. We have used a magnesium loading-test to examine the relationship between ventricular ectopy and magnesium status in 14 digitalised patients with chronic AF. Among seven patients with infrequent VPB (less than 250 24 h-1; mean 107 24 h-1) mean magnesium retention was 10.1% and four subjects retained no significant quantities of magnesium, indicating magnesium repletion. Among the remaining seven patients, mean magnesium retention was significantly higher (33.1%, P less than 0.02) and all patients retained 20% or more of the load given. There was an overall relationship between Mg retention and numbers of VPB (rs = 0.54; P less than 0.05). Magnesium deficiency may be determinant of ventricular ectopy in digitalised patients with chronic AF.

Aged↗
PubMed1990

[Magnesium deficiency dermatitis--changes in leukotriene levels and effects of azelastine hydrochloride on the dermatitis and leukotriene B4].

To estimate the pathogenesis of magnesium deficiency dermatitis (MDD) in the hairless rats fed with a hypomagnesic diet, plasma concentrations of leukotrienes (LTB4, LTC4, LTD4) were measured. Inhibitory effect of azelastine hydrochloride (AZ), which is known as an inhibitor of 5-lipoxygenase, on MDD was also evaluated. In the hairless rats with magnesium deficiency condition, plasma level of leukotriene B4 was increased, whereas LTC4 and LTD4 showed no changes. In AZ-administered rats, MDD was depressed with the dose-dependent tendency. However, the decrease of LTB4 level did not follow therapeutic effect of AZ for gross appearance of dermatitis. These results indicated that development of MDD associates with increase of LTB4, but its pathogenetic role still remains unknown, and inhibitory effect of AZ against MDD not based on reduction of LTB4 production.

Animals↗
PubMed2005

Magnesium deficiency impairs fear conditioning in mice.

Magnesium (Mg2+) is one of the most abundant cations found in the body. In the central nervous system, Mg2+ plays an important role in the function of N-methyl-D-aspartate (NMDA)-type glutamate receptors, which are centrally involved in memory processing. Despite the relatively large concentration of Mg2+ in the CNS, little is known about the behavioral consequences of Mg2+ deficiency. The purpose of this study was to address this issue by assessing fear conditioning and related behaviors in mice maintained on normal or Mg(2+)-deficient diets. Young adult male C57Bl/6J mice were placed on a control or Mg(2+)-deficient diet, and testing was conducted between 10 and 21 days later. Magnesium-deficient mice exhibited impairments in contextual and cued fear conditioning. These impairments could not be attributed to changes in locomotor activity, exploration, or pain sensitivity. Furthermore, Mg(2+)-deficient mice were more sensitive to the convulsant effects of a peripheral injection of NMDA (100 mg/kg, IP). The results suggest that magnesium deficiency can lead to specific impairments in emotional memory. Such impairments may be related to hypersensitivity of NMDA-type glutamate receptors in Mg(2+)-deficient mice.

Animals↗
PubMed2003

Magnesium-deficient medium enhances NO production in alveolar macrophages isolated from rats.

Magnesium deficiency has been shown to increase nitric oxide (NO) levels in plasma and to aggravate endotoxin lethality. The present study was performed to examine the effects of magnesium (Mg(2+))-deficient culture medium, with and without endotoxin (LPS), on NO release and inducible NOS (iNOS) mRNA levels in alveolar macrophages isolated from rats. Decreasing the Mg(2+) concentration in the culture medium from 0.39 mM (normal-Mg(2+) medium) to 0.021 mM (Mg(2+)-deficient medium) increased NO release from alveolar macrophages for 2 h. However, LPS stimulation in Mg(2+)-deficient medium had little effect on NO release. The increased NO release in Mg(2+)-deficient medium was suppressed completely by L-NAME and aminoguanidine. Dexamethasone, pyrrolidine dithiocarbamate and curcumin strongly inhibited NO release. Verapamil, U73122, TMB-8 and W-7 had no significant effect on NO release induced by Mg(2+) deficiency. Preculture of macrophages with Mg(2+)-deficient medium for 22 h markedly increased NO release and iNOS mRNA levels for a further 2 h; these increments were suppressed completely by curcumin. These results suggest that Mg(2+) deficiency enhances NO production via iNOS by alveolar macrophages. In this experimental condition, we can not suggest that NO production from alveolar macrophage plays an essential role in the pathogenesis of enhanced endotoxin lethality in Mg-deficient rats.

Animals↗
PubMed1982

Magnesium requirement of fingerling channel catfish and signs of magnesium deficiency.

Purified casein diets with and without supplemental magnesium were fed to fingerling channel catfish (Ictalurus punctatus) in order to establish the essentially of this mineral. Fish fed the basal diet containing 0.004% magnesium developed deficiency signs such as poor growth, anorexia, sluggishness, muscle flaccidity and high mortality. After 3 weeks, two groups of fish fed the basal diet were converted to the supplemental diet containing 0.057% magnesium. Deficiency signs in these fish were alleviated almost immediately. In a second experiment, graded levels of magnesium sulfate were added to casein-based diets and fed to channel catfish fingerlings to determine their dietary requirement for magnesium. Results indicated that a minimum magnesium level of 0.04% of the dry diet was required to maintain normal growth, serum and bone magnesium levels in channel catfish fingerlings.

Animals↗
PubMed1976

Impaired release of parathyroid hormone in magnesium deficiency.

Parathyroid hormone release and end-organ responsiveness to parathyroid extract (PTE) were evaluated in a 25-year-old woman with magnesium deficiency associated with hypocalcemia and inappropriately low levels of serum immunoreactive parathyroid hormone (iPTH). End-organ responsiveness to PTE was demonstrated by increases in serum calcium and in urinary phosphorus, cyclic AMP, and hydroxyproline. When the serum calcium was increased from a baseline of 6.9 mg/100 ml to levels of 8.0 mg/100 ml and higher by calcium infusion, the serum iPTH decreased from the low normal range to below the limits of detectability. The intravenous administration of 3 mg/kg of body weight of magnesium led to an abrupt and striking increase in circulating iPTH with a 2-fold increase in one minute, a 6-fold increase in two minutes, and an 8-fold increase in five minutes. The very rapid increase in serum iPTH produced by magnesium infusion in this study suggests an effect of magnesium on hormone secretion rather than an effect on hormone synthesis. The evidence provided by this investigation indicates that the release of parathyroid hormone is impaired in magnesium deficiency and that the level of circulating calcium required for the suppression of parathyroid hormone secretion is lower than that in normal subjects.

Adult↗