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PubMed1983

Magnesium deficiency after ileal resections for Crohn's disease.

The magnesium status of the body was studied in 87 patients with various lengths of small-bowel resections for Crohn's disease. The urinary magnesium excretion decreased with increasing resection length, and so did the concentration of magnesium in muscle. Muscular fatigue, an early symptom of magnesium deficiency, was positively correlated to a pathologically low concentration of muscle magnesium. It was concluded that clinically important magnesium deficiency, which was not detected by determination of serum magnesium, occurred in patients with ileal resections exceeding 75 cm.

Adult↗
PubMed1979

Cell population kinetics and biochemical changes in the rat stomach during magnesium deficiency.

Cell populations of rat stomach have been counted following varying (4-60 days) periods of magnesium-deficient diet and compared to a control group. The activity of beta-glucuronidase and the serotonin concentration were assayed in magnesium-deficient and control rats within four weeks. In the rat stomach the magnesium deficiency produces a numerical decrease in mucous cells, especially marked after 3 and 4 weeks. At this time, the activity of beta-glucuronidase decreases significantly. The concentration of serotonin increases at an earlier time and this increase coincides with the onset of the typical erythema occurring in magnesium-deficient rats.

Animals↗
PubMed1999

Gestational magnesium deficiency is deleterious to fetal outcome.

A number of recent epidemiological findings have implicated magnesium as being essential to fetal well-being. Few studies, however, have examined the relationship between maternal requirements for dietary magnesium and subsequent mortality and morbidity in offspring. The present study uses a rodent model of dietary-induced hypomagnesemia to investigate the effects of magnesium deficiency prior to and during gestation on neonatal morbidity and mortality. Magnesium deficiency during gestation significantly increased neonatal mortality and morbidity. Such increases were associated with a reduced free magnesium concentration in both maternal and offspring blood and an increased incidence of periventricular hemorrhage and edema in newborn pups as observed by magnetic resonance imaging and histology. Animals fed a magnesium-deficient diet before mating but given magnesium supplementation during gestation did not demonstrate a significant change in neonatal mortality and morbidity when compared to control animals. The significant improvement in fetal outcome with dietary magnesium supports the concept of magnesium supplementation during pregnancy.

Animals↗
PubMed1983

The effect of magnesium deficiency on glucose stimulated insulin secretion in rats.

Weanling Sherman rats were pair-fed for 8 days on a control or a magnesium deficient diet containing 70.5% sucrose. After a 12-hour fast, the rats were injected intraperitoneally with glucose (250 mg/100 g body weight) and arterial blood was drawn at 0, 15, 30, 60, 90 minutes after injection. Before glucose loading, in magnesium deficient rats, plasma magnesium levels were significantly increased. The plasma triglyceride concentration was significantly higher in magnesium deficient rats compared to controls. After glucose loading, in the control group, the plasma insulin concentrations increased to 67.9 +/- 5.8 microU/ml at 15 minutes and returned to pretreatment levels by 30 minutes; in the magnesium-deficient rats, the plasma insulin levels were significantly lower at 15 minutes 32.9 +/- 5.6 microU/ml (P less than 0.01) and returned more slowly to the pre-challenge level. No significant differences were observed in plasma glucose levels between the two groups of rats.

Animals↗
PubMed2001

Effects of enrofloxacin and magnesium deficiency on matrix metabolism in equine articular cartilage.

OBJECTIVE: To investigate the effects of enrofloxacin and magnesium deficiency on explants of equine articular cartilage. SAMPLE POPULATION: Articular cartilage explants and cultured chondrocytes obtained from adult and neonatal horses. PROCEDURE: Full-thickness explants and cultured chondrocytes were incubated in complete or magnesium-deficient media containing enrofloxacin at concentrations of 0, 1, 5, 25, 100, and 500 microg/ml. Incorporation and release of sulfate 35S over 24 hours were used to assess glycosaminoglycan (GAG) synthesis and degradation. An assay that measured binding of dimethylmethylene blue dye was used to compare total GAG content between groups. Northern blots of RNA from cultured chondrocytes were probed with equine cDNA of aggrecan, type-II collagen, biglycan, decorin, link protein, matrix metalloproteinases 1, 3, and 13, and tissue inhibitor of metalloproteinase 1. RESULTS: A dose-dependent suppression of 35S incorporation was observed. In cartilage of neonates, 35S incorporation was substantially decreased at enrofloxacin concentrations of 25 mg/ml. In cartilage of adult horses, 35S incorporation was decreased only at enrofloxacin concentrations of > or =100 microg/ml. Magnesium deficiency caused suppression of 35S incorporation. Enrofloxacin or magnesium deficiency did not affect GAG degradation or endogenous GAG content. Specific effects of enrofloxacin on steady-state mRNA for the various genes were not observed. CONCLUSION AND CLINICAL RELEVANCE: Enrofloxacin may have a detrimental effect on cartilage metabolism in horses, especially in neonates.

Age Factors↗
PubMed1994

Magnesium deficiency as a cause of hypocalcemia in the CHARGE association.

OBJECTIVE: To discover the mechanism of hypocalcemia in a patient with the CHARGE (coloboma, heart disease, atresia choanae, retarded growth and development, genital hypoplasia, and ear anomalies) association. RESEARCH DESIGN: Chemical and metabolic studies of serum, urine, stool, and muscle specimens. SETTING: A university hospital affiliated with a municipal hospital. PARTICIPANT: One patient with the CHARGE association and refractory hypocalcemia. MEASUREMENTS AND RESULTS: Serum calcium level was 0.91 mmol/L (reference range, 2.20 to 2.58 mmol/L) and serum magnesium level was 0.34 mmol/L (reference range, 0.80 to 1.20 mmol/L) prior to any therapy. After parenteral calcium and magnesium therapy, hypocalcemia persisted (1.46 mmol/L), while the serum magnesium level was 0.84 mmol/L. A needle biopsy of skeletal muscle tissue for the magnesium content confirmed a total magnesium deficiency despite normomagnesemia (muscle magnesium content, 517 micrograms/g [reference range, 800 to 1100 micrograms/g]). Magnesium deficiency was secondary to secretion of magnesium into the gastrointestinal tract (with a daily magnesium intake of 190 mg, a 24-hour nondiarrheal fecal excretion of magnesium was 2019 mg/kg [reference range, < 1000 mg/kg of stool weight]). INTERVENTIONS: Hypocalcemia was corrected only after 7 weeks of continual parenteral magnesium supplements to replenish the tissue magnesium deficiency. CONCLUSIONS: Patients with the CHARGE association often have hypocalcemia. Magnesium deficiency (with or without hypomagnesemia) is a cause of the hypocalcemia in at least one patient and may prove of significance in others.

Abnormalities, Multiple↗
PubMed1994

Magnesium-deficiency potentiates free radical production associated with postischemic injury to rat hearts: vitamin E affords protection.

Preexisting magnesium deficiency may alter the susceptibility of rat hearts to postischemic oxidative injury (free radicals). This was examined in rats maintained for 3 weeks on a magnesium-deficient (Mg-D) diet with or without concurrent vitamin E treatment (1.2 mg/day, SC). Magnesium-sufficient (Mg-S) rats received the same diet supplemented with 100 mmol Mg/kg feed. Following sacrifice, isolated working hearts were subjected to 30-, 40-, or 60-min global ischemia and 30-min reperfusion. Postischemic production of free radicals was monitored using electron spin resonance (ESR) spectroscopy and spin trapping with alpha-phenyl-N-tert butylnitrone (PBN, 3 mM final); preischemic and postischemic effluent samples were collected and then extracted with toluene. PBN/alkoxyl adduct(s) (PBN/RO.; alpha H = 1.93 G, alpha N = 13.63 G) were the dominant signals detected in untreated Mg-S and Mg-D postischemic hearts, with comparably higher signal intensities observed for the Mg-D group following any ischemic duration. Time courses of postischemic PBN/RO. detection were biphasic for both groups (maxima: 2-4 and 8.5-12.5 min), and linear relationships between the extent of PBN/RO. production and the severity of both mechanical dysfunction and tissue injury were determined. Following each duration of ischemia, Mg-D hearts displayed greater levels of total PBN adduct production (1.7-2.0 times higher) and lower recovery of cardiac function (42-48% less) than Mg-S hearts. Pretreating Mg-D rats with vitamin E prior to imposing 40-min ischemia/reperfusion, led to a 49% reduction in total PBN/RO. production, a 55% lower LDH release and a 2.2-fold improvement in functional recovery, compared to untreated Mg-D hearts. These data suggest that magnesium deficiency predisposes postischemic hearts to enhanced oxidative injury and functional loss, and that antioxidants may offer significant protection against the pro-oxidant influence(s) of magnesium deficiency.

Animals↗
PubMed1981

Magnesium deficiency. Etiology and clinical spectrum.

Magnesium deficiency may complicate many diseases. The causes include the following: inadequate intake during starvation or increased requirement during early childhood, pregnancy, or lactation; excessive losses of magnesium as a result of malabsorption from the gastrointestinal tract or from the kidneys during use of diuretics; and to a combination of the two, as in alcoholism. Most often the etiological factors have been operative for a month or more. Acute hypomagnesemia can occur without previous Mg deficiency after epinephrine, cold stress and stress of serious injury or extensive surgery. The clinical manifestations depend on the age of the patient and may begin insidiously or with dramatic suddenness, or there may be no overt symptoms or signs. The manifestations can be divided into the following categories: totally non-specific symptoms and signs ascribable to the primary disease; neuromuscular hyperactivity including tremor, myoclonic jerks, convulsions, Chvostek sign, Trousseau sign (rarely), spontaneous carpopedal spasm (rarely), ataxia, nystagmus and dysphagia; psychiatric disturbances from apathy and coma to some of all facets of delirium; cardiac arrhythmias including ventricular fibrillation and sudden death; hypocalcemia which is responsive only to Mg therapy; and hypokalemia which is not easily nor completely corrected without Mg therapy. The diversity of etiologies and the multiplicity of manifestations result in confusion and controversy. The documentation of normal renal function is absolutely necessary for maximum doses. The order of magnitude of dose is 1.0 meq Mg/kg on day 1, and 0.3 to 0.5 mEq/kg per day for 3 to 5 days. In emergencies such as convulsions or ventricular arrhythmias, a bolus injection of 1.0 gm (8.1 meq) of MgSO4 is indicated. Therapy of Mg deficiency in the presence of renal insufficiency requires smaller doses and frequent monitoring. Complete repletion occurs slowly.

Adolescent↗
PubMed1982

Effects of magnesium deficiency on intratubular calcium oxalate formation and crystalluria in hyperoxaluric rats.

Previous studies have shown that magnesium deficiency accelerates renal tubular calcium oxalate monohydrate deposition in rats on chronic hyperoxaluric, lithogenic protocols. The present study was conducted to investigate the effect of magnesium deficiency on intratubular calcium oxalate formation in rats from the 1st day of administration of a hyperoxaluric agent. The objectives were to delineate early ultrastructural features of the formation, mechanisms of retention, and development of renal tubular crystal deposits and to characterize the crystalluria in rats on the hyperoxaluric/hypomagnesuric protocol. Intratubular calcium oxalate monohydrate deposits were found in magnesium deficient rats after only 24 hours of ad libitum administration of 1 per cent ethylene glycol drinking water. Animals on regular food diet did not display renal tubular deposition after 11 days of ethylene glycol administration. Strand- and sheet-like organic material emanating from the luminal wall of the tubules was adherent to the crystals, thereby serving to immobilize them within the tubule. Calcium oxalate monohydrate crystals predominated in the urines of hyperoxaluric/hypomagnesuric animals with intratubular deposits while dihydrate crystals were the primary constituent of urines from rats administered ethylene glycol alone (no intratubular deposition). The results support the supposition that under certain conditions magnesium deficiency is a significant risk factor for intrarenal calcium oxalate deposition and stone formation. Furthermore the identification of calcium oxalate monohydrate crystalluria may be an important indicator of the propensity toward intranephronic calcium oxalate formation and urolithiasis.

Animals↗
PubMedDate not supplied

[Pathophysiology and therapy of magnesium deficiency in pregnancy].

We determined serum magnesium(Mg)-levels in 67 pregnant women in late pregnancy. 42 gravidae complained of nightly muscle cramps; 21 of them received 1.8 g monomagnesiumaspartate twice daily per mouth for 4 weeks. 2 and 4 weeks after the initiation of therapy serum Mg-levels were again determined. Serum Mg-levels were lower in pregnant women as compared to a control group of non pregnant women. Gravidae complaining of muscle cramps had significantly lower serum Mg-levels than women without muscle cramps. The administration of Mg was associated with a significant rise in serum Mg-levels as early as 2 weeks after the initiation of therapy. Our study indicates that nightly muscle cramps during pregnancy might be a sign of a latent magnesium deficiency which can be influenced by oral magnesium.

Adult↗
PubMed1982

Magnesium deficiency in chronic alcoholic patients uncovered by an intravenous loading test.

Magnesium sulphate (30 mmol in 1 litre NaCl solution, 154 mmol/l) was infused over 8 h i.v. in overnight fasted reference group (n = 12) and chronic alcoholics (n = 16) with normal kidney function. The magnesium excreted in the urine was measured in the 24 h urine beginning at the start of the infusion. Alcoholics excreted 1-15 mmol magnesium (median 6.4) and the reference group 18-30 (median 23.2) in the 24 h after the load. When the loading was repeated in the alcoholics (n = 7) after having received a hospital diet supplemented with 150 mmol magnesium citrate for 10 days, the elimination in the urine increased from 1-12 mmol (median 6.1) to 14-25 (median 20.8) close to the results in the reference group. The elimination in the urine was highly correlated (rs = 0.7) to the serum albumin concentration. The amount of magnesium eliminated in the urine by the reference group and the chronic alcoholic patients did not correlate with their serum concentrations of magnesium. The magnesium loading test in adults clearly separates a reference group from the magnesium deficient chronic alcoholics and can be used both for the diagnosis of magnesium deficiency and to follow the individual patient during repletion.

Alcoholism↗
PubMed1975

Postoperative magnesium deficiency.

Prolonged nasogastric suction and the administration of magnesium-free parenteral fluids produced magnesium deficiency in a patient in the postoperative period. The symptoms of magnesium deficiency are usually overshadowed by those of the primary disease and diagnosis usually rests on the demonstration of low blood concentrations of the ion. Magnesium replacement must be kept in mind when treating patients with intravenous fluids for prolonged periods.

Colectomy↗
PubMed2006

[Potentiation of Delta9-tetrahydrocannabinol (THC) effects by magnesium deficiency in the rat].

Aggressive behavior can be classified into three major categories: defense, social attack and predatory behavior. The predatory behavior of rats, which prompts them to prey on mice (muricidal behavior) may be induced by injection of high doses (11 mg/kg) of Delta9-tetrahydrocannabinol (THC) or by acute magnesium deficiency. We have studied the effect of a single injection of low doses of THC (2, 4 or 8 mg/kg) in rats with a severe (50 ppm magnesium diet) or moderate (150 ppm) magnesium deficiency. The combination of moderate magnesium deficiency with low doses of THC induced muricidal behavior in all the rats and an increase in aggressiveness at the doses of 4 or 8 mg/kg of THC. Hyperaggressiveness increased with magnesium deficiency severity. Serotonin is probably involved in aggressiveness induced by both moderate magnesium deficiency and low doses of THC, but implication of other neurotransmitters and magnesium deficiency-induced alterations of CB1-and/or CB2-receptor expression are not excluded.

Aggression↗
PubMed1993

Do diuretics cause magnesium deficiency?

1. Controlled trials, of which there are few, do not substantiate claims that diuretics play a role in causing magnesium deficiency. Consequently, the vast majority of patients taking conventional doses of thiazide diuretics (i.e. bendrofluazide 2.5 mg day-1 or equivalent) do not need magnesium supplements. On balance, potassium-sparing diuretics tend to increase serum and intracellular magnesium content; this should not be taken as evidence of prior magnesium deficiency. It remains theoretically possible that large doses of loop diuretics given more than once daily for long periods could induce negative magnesium balance and magnesium deficiency. However, it has been difficult to run appropriately controlled trials in conditions where such therapy is needed (i.e. heart failure) and until more reliable information becomes available no absolute recommendation can be made. 2. Methods for the measurement of intracellular free magnesium levels are now available and are more relevant to the assessment of magnesium deficiency than total intracellular magnesium content; the complex relationship between intracellular free and total magnesium content remains to be defined. Future work involving the effect of diuretics on intracellular free magnesium measurements should make every attempt to avoid the errors of trial design and multiple publication that litter current and past literature.

Animals↗
PubMed1975

Skeletal effects of magnesium deficiency in normal, ovariectomized, and estrogen-treated rats.

The effects of magnesium deficiency in ovariectomized and estrogen-treated rats were examined in histological sections of bones and various soft tissues. The changes observed in the femora of intact rats deprived of magnesium for three weeks were: 1. a general increase in diaphyseal thickness, 2. the presence of localized fibrous or bony-like masses in subperiosteal and metaphyseal sites, and 3. the occurrence, although rare, of endosteal hyperplasia. In ovariectomized, magniesium-deprived animals, the incidence and location of fibrous masses were similar to that in the femora of magnesium-deficient intact rats; however, no increase in diaphyseal thickness was noted. Daily injections of 25 mug estradiol caused a reduction of the frequency of skeletal hyperplasia from 80% to 20%, as well as a reduction in femoral diaphyseal thickness. Estradiol hormone administration also brought about a marked alleviation of the dermal and neural manifestations of magnesium deficiency, but, at the same time, caused an exacerbation of renal calcinosis.

Animals↗
PubMed2001

Biochemical changes in Achilles tendon from juvenile dogs after treatment with ciprofloxacin or feeding a magnesium-deficient diet.

Quinolones are antibacterial agents that have the potential to induce Achilles tendon disorders - such as tendinitis or even ruptures - in patients treated with these drugs. We studied the effects of ciprofloxacin on several proteins of Achilles tendons from immature dogs, 10- to 11-weeks-old. The dogs were treated orally for 5 days with 30 or 200 mg ciprofloxacin/kg body weight or with the vehicle alone. Since quinolone-like alterations in joint cartilage were observed in magnesium-deficient animals, another group was fed a magnesium-deficient diet for 6 weeks. At necropsy, tendons (n=3 from each group) were frozen and stored until analysis when they were homogenized in a lysis buffer to release a soluble fraction of the tendon proteins. Densitometric analysis of the immunoblots with anticollagen type I, anti-elastin, anti-fibronectin, and antiintegrin antibodies showed a significant reduction of all proteins. For example, collagen type I concentrations (mean +/-SD, arbitrary densitometric units) were 3190+/-217 (controls), 1890+/-468 (30mg/kg), 1695+/-135 (200mg/kg) and 2053+/-491 in the magnesium-deficient dogs. The differences between concentrations in controls and all treated groups were statistically significant (P<0.01, t-test). Similarly, compared with control samples, relative concentrations of other proteins in tendons from ciprofloxacin-treated dogs (30 mg/kg) decreased by 73% (elastin), 88% (fibronectin), and 96% (beta1 integrin) (data from low-dose group only). A very similar pattern of protein alterations was detected in samples from magnesium-deficient dogs. In conclusion, rather low doses of a fluoroquinolone or a diet-induced magnesium deficiency caused similar biochemical alterations in the soluble fraction of proteins from canine tendons. These findings support our hypothesis that quinolone-induced toxic effects on connective tissue structures are due to the magnesium-antagonistic effects of these antibacterial agents. They also indicate that patients with a latent magnesium deficiency could be at an increased risk of quinolone-induced tendon disorders.

Achilles Tendon↗
PubMed1994

Neurogenic peptides and the cardiomyopathy of magnesium-deficiency: effects of substance P-receptor inhibition.

Dietary deficiency of magnesium (Mg) in rodents results in cardiomyopathic lesion formation. In our rat model, these lesions develop after 3 weeks on the Mg-deficient diet; significant elevation of several cytokines, IL-1, IL-6 and TNF alpha also occurs. In probing the mechanisms of lesion formation, we obtained data supporting the participation of free radicals (Freedman AM et al.: Bioch Biophys Res Commun 1990; 170: 1102). Recently, we identified an early elevation of circulating substance P and proposed a role of neurogenic peptides during Mg-deficiency (Weglicki WB, Phillips TM: AM J Phys 1992;262:R734). The present study was designed to evaluate the contribution of neurogenic peptides to the pathogenesis of Mg-deficiency. In the blood, substance-P and calcitonin gene related peptide (CGRP) are elevated during the first week on the diet. During the second week, circulating histamine, PGE2 and TBAR-materials were elevated and red cell glutathione was reduced, all prior to the elevation of the inflammatory cytokines during the third week. When the rats were treated with the substance P-receptor blocker [CP-96,345], the levels of substance P and CGRP remained elevated; however, increases in histamine, PGE2, TBAR-materials, and the decrease in red cell glutathione were inhibited; also, the development of cardiac lesions was inhibited significantly. These data support a central role for neurogenic peptides, especially substance P, in the development of cardiomyopathic lesions during Mg-deficiency.

Animals↗
PubMed1997

[Effects of dietary magnesium deficiency in the rat: with special reference to ultrastructural examination].

Epidemiologically, it has been suggested that dietary magnesium/calcium imbalance is associated with the risk of heart diseases. In the present study, the effects of magnesium deficiency and/or calcium over intake were investigated in rats. Male Sprague-Dawley rats were divided into 4 groups, and respectively fed basal diet (AIN-76) alone (Group 1), calcium-doubled AIN-76 diet (Group 2), magnesium-deficient AIN -76 diet (Group 3) and magnesium-deficient/calcium-doubled AIN-76 diet (Group 4) for 19 days. A biochemical assay using inductively coupled plasma showed that the magnesium concentrations of the femoral bone and serum were significantly (p < 0.001) lower in Groups 3 and 4 than in Group 1. The lipid peroxides of the heart in Group 4 and of the liver in Groups 3 and 4 were increased as compared to the Group 1 values although there was no statistical significance. Ultrastructurally, degenerative changes of organellas including mitochondria were observed in myocardial, liver and renal tubule cells of Groups 2-4. Severe degeneration such as disorganization, lysis and disarrangement of myofibrils was most evident in myocardial cells of Group 4. Our results thus suggest that dietary magnesium deficiency gives rise to retrogressive changes in some organs including the heart, and concurrent calcium overintake synergistically enhances the myocardial injury due to magnesium deficiency.

Animals↗