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PubMed1985

Renal magnesium and phosphate wastage in a patient with hypercalciuria and nephrocalcinosis: effect of oral phosphorus and magnesium supplements.

We report a 29-year-old man with a mild decrease in glomerular filtration, nephrocalcinosis, hypercalciuria and a renal magnesium leak. He had other features of 'congenital magnesium-losing kidney', such as arthritis and hyperuricemia, short stature and recurrent urinary tract infections, but had no radiological chondrocalcinosis. In addition, pallidal calcification was found. The patient also had a renal phosphate leak. Phosphorus supplements resulted in a decrease in urinary calcium excretion, indicating that hypercalciuria was at least partially a consequence of phosphorus depletion. Plasma and urine magnesium were not affected by phosphorus supplements. Addition of magnesium supplements resulted in a transient and modest decrease in urinary calcium excretion, with no modification in plasma magnesium.

Administration, Oral↗
PubMed1991

Magnesium intoxication in a neonate from oral magnesium hydroxide laxative.

This is a case of magnesium intoxication in a neonate produced by an oral magnesium cathartic. A review of the literature revealed there are very few cases that have been reported of magnesium toxicity due to cathartics. There is no recommended dose for magnesium cathartics in neonates or data on their safety. A review of the management of magnesium intoxication is presented.

Administration, Oral↗
PubMed1999

The possible role of magnesium in protection of premature infants from neurological syndromes and visual impairments and a review of survival of magnesium-exposed premature infants.

The survival rate of very preterm, low birth weight infants (weighing less than 1500 g) is 85 per cent in the USA and is ever increasing, while 42 to 75 per cent of extremely premature infants (weighing 751-1000 g) survive. Of great concern is the lack of consistent decrease in neurological syndromes and associated visual impairments. Because of short gestations, these infants have not had time to accrue up to 80 per cent of magnesium normally present at term. These very preterm infants are at highest risk for cerebral hypoxia/ischemia (H/I), intracranial hemorrhage (ICH), periventricular leukomalacia (PVL) or cystic PVL (CPVL), and possible sequelae, cerebral palsy (CP) and mental retardation (MR). These syndromes are associated with damage to optic structures and the visual pathways which traverse the brain. Visual defects are common in surviving preterm infants. Increased levels of harmful neurochemical mediators that have been reported in these conditions include oxygen free radicals, excitatory amino acids, tumor necrosis factor-alpha (TNF-a), and thromboxane A2 (TXA2) which are aggravated in magnesium deficiency and may be ameliorated by magnesium. We review the published data concerning the effects of prenatal magnesium supplementation on ICH, CPVL, CP and MR and available reports concerning survival. Further considerations on the safety and efficacy of magnesium sulphate administration given prenatally to the preterm neonate await the outcome of three trials that are continuing for more than a year on three continents.

Humans↗
PubMed2002

Effects of high doses of magnesium in drinking water and voluntary wheel running on magnesium and calcium concentrations in rats.

The effect of high magnesium intake in addition to supplementation and voluntary wheel activity on magnesium and calcium homeostasis was investigated in rats. Thirty-six 5-week-old male Wistar rats were divided into four groups (n = 9). Groups 2 and 4 received five hundred ppm of elemental magnesium as MgCl2 provided in drinking water. After 1 week of acclimatization and 4 weeks of supplement and/or exercise, the animals were fasted and sacrificed. It appears that magnesium supplementation as well as exercise played some significant role in the homeostatic changes of magnesium and calcium. This could be of great significance in better understanding of mineral homeostasis particularly in sports medicine.

Animals↗
PubMed1991

Magnesium transport in human pregnancy (magnesium content of human gestation tissues and tissue fluids).

Authors used atom absorption spectrophotometry to determine the magnesium content of gestation tissues (placenta, myometrium) and tissue fluids (maternal blood, cord blood, amniotic fluid) taken in different periods of gestation. Magnesium concentration was found higher in the cord blood than in the maternal serum. It was assumed that the concentration gradient between mother and fetus resulted from active transport. There was a significant difference between the magnesium content of the amniotic fluid and the cord blood sera (P < 0.001). The magnesium content of the mature chorion tissue was by nearly 40% lower than that of the immature one. The magnesium content of the myometrium decreased by 38% by Week 40 of gestation, as compared to the value in Week 37.

Amniotic Fluid↗
PubMed1990

Competitive inhibition of magnesium-induced [3H]N-(1-[thienyl] cyclohexyl)piperidine binding by arcaine: evidence for a shared spermidine-magnesium binding site.

The polyamine competitive antagonist arcaine (1,4-diguanidino-butane) produced complete inhibition of basal [3H]N-(1-[thienyl] cyclohexyl)piperidine ([3H]TCP) binding, with an IC50 value of 4.52 +/- 0.93 microM. Arcaine (5 and 10 microM) produced a decrease in the affinity without a significant change in the receptor density of [3H]TCP binding under equilibrium conditions. In addition, arcaine did not alter either N-methyl-D-aspartate-specific [3H] glutamate or strychnine-insensitive [3H]glycine binding. Furthermore, increasing concentrations of arcaine produced parallel rightward shifts in the concentration-response curves for both spermidine- and magnesium-induced [3H]TCP binding, suggesting that arcaine is a competitive inhibitor of both agonists. Similar rightward shifts were observed for barium- and strontium-induced [3H]TCP binding. In contrast, arcaine decreased the efficacy of glutamate- and glycine-induced [3H]TCP binding without changing their EC50 values, indicating a noncompetitive type of inhibition. These results imply that spermidine and certain divalent cations including magnesium share the same mechanism for enhancing [3H]TCP binding, whereas glutamate and glycine have different sites of action. This is further supported by the additive effect of spermidine when tested in the presence of maximal concentrations of glutamate and glycine. On the other hand, spermidine and magnesium were not additive and, in fact, magnesium was able to block the effects of spermidine under certain conditions. The possibility that magnesium is a partial agonist at the polyamine site is discussed.

Animals↗
PubMed1989

[The significance of magnesium in orthopedics. V. Magnesium in osteoporosis].

The authors submit an investigation of 60 patients with senile, post-menopausal and drug-induced osteoporosis. Using the method of absorption spectrophotometry, they found a reduced level of Mg in red blood cells in 63.6% of senile, 66.7% postmenopausal and only in 22.2% drug-induced osteoporoses. Also the mean level of red cell magnesium was significantly lower in the group of senile (1.94 mmol) and postmenopausal (1.85 mmol) osteoporosis as compared with drug-induced osteoporosis (2.25 mmol). The authors revealed moreover that the level of red cell magnesium in the former two groups declines in proportion to the severity of osteoporosis and correlates thus with the clinical and X-ray finding. For treatment of osteoporisis the authors used magnesium lactate alone (in 37 patients) and combined with sodium fluoride (in 23 patients). In the majority of patients they had very favourable results. Based on laboratory and therapeutic results, consistent with data in the experimental literature, the authors assume that magnesium as a catalyst of bone metabolism and as one of the most important factors controlling the formation of bone matrix and its mineralization plays a significant role in the aetiopathogenesis of senile and postmenopausal osteoporosis. The authors assume that Mg deficiency which is increasing in recent years in soil as well as in foodstuffs and water may be the main cause of the increasing number of patients with osteoporosis in civilized countries. Magnesium should have its firm place not only in therapy but also in prevention of the majority of osteoporosis.

Aged↗
PubMedDate not supplied

[The importance of betamimetics and magnesium for the outcome of pregnancy: I. Reduction of intrauterine growth retardation, premature rupture of membranes and premature birth after supplemental magnesium therapy].

Of 4 905 single pregnancies recorded within a 4 year period (1979-1982) 882 (18%) were risk pregnancies managed with Betamimetics (B); of these 348 (7,1%) had tocolysis (T) and 534 (10,9%) tocolysis and cerclage (T/C). Since the end of 1979 the patients received in addition to the Betamimetic a K-Mg-Vitamin drug (Feto-Longoral) aimed at "Cardioprotection", and since the beginning of 1981 30-40 mval oral Mg daily in the form of Magnesium aspartate (Mg 5-Longoral) to "support tocolysis". The mean age, parity, percentage with Magnesium therapy, the pregnancy outcome using a gestational age limit less than or equal to 36 weeks, the frequency of premature ruptured membranes (PROM) in premature and mature infants as well as the number of intrauterine growth retarded infants (IUR) (less than 10th percentile BPE) were yearly evaluated and compared for both risk collectives T and T/C as well as for the normal collectives (N). While only 2% of the normal collectives had a pregnancy duration of less than or equal to 36 weeks (completed) the figure was five fold in both T and T/C groups, and however was yearly reduced in the T/C group from 11,0% (1979) to 4,9% (1982). The frequency of PROM with premature infants in the T and T/C groups is about 6% (N-collectives about 1%). It is however reduced in the T/C group in 1981 to 2,2% and in 1982 to 1,6%. For mature infants it is N: 17-12% (fluctuating) and B (T + T/C): 22-11% (yearly decreasing). The rate of IUR (less than 10th percentile BPE) in the T and T/C groups in 1979 was 22,2 and 20,5% respectively and in 1980 12,6 and 17,5% respectively. It is further reduced in 1981 to 11,6 and 8,8% respectively and in 1982 to 9,7 and 10,6% respectively (N-collectives between 8,3 and 11,5%). The "weight gain" exceeds the 25th percentile (Hohenauer): 1979 and 1980 for B: 33,1 and 30,2% respectively, and 1981 and 1982 for B: 25,4 and 24,2% respectively (N between 26,5 and 19,5%). The results show that patients with tocolysis--with or without cerclage--have more premature and growth-retarded infants than normal collectives (a sign of more placenta insufficiencies). In the two years where Magnesium was supplemented at 30-40 mval daily, short term pregnancies, the PROM frequency and the IUR rate decreased (statistically evaluated). It could thus be concluded that a relative Magnesium deficiency might have been responsible for a certain percentage of premature births and hypotrophic infants and that better results were obtained after Magnesium substitution.

Adrenergic beta-Agonists↗
PubMed1984

Inhibition of calcium by magnesium in the contraction of rat aortic smooth muscle. I. Mathematical model of calcium and magnesium binding.

A mathematical model of the effect of calcium and magnesium binding on muscle tension was developed. The model was tested on aortic smooth muscle tissue obtained from rats fed magnesium-sufficient (Mg: 650 ppm) and magnesium-deficient (Mg: 4.5 ppm) diets. Ca2+ binding constants of 2.51 X 10(3) and 2.3 X 10(3) M-1 were obtained for aortae from magnesium-sufficient and magnesium-deficient rats, respectively. The corresponding Mg2+ binding constants were 0.6 X 10(3) and 0.4 X 10(3) M-1. The data indicate that Mg2+ is a competitive inhibitor of Ca2+ in tension development in rat aortic smooth muscle tissue.

Animals↗
PubMed1993

A physiological oral magnesium supplement does not influence total serum magnesium, left ventricular ejection fraction and prognosis in patients with dilated cardiomyopathy.

It has been postulated that patients with congestive heart failure (CHF) benefit from physiological oral magnesium supplements. In order to study the effect of such supplements upon patients with idiopathic dilated cardiomyopathy (IDC) we studied a group of 23 patients with the salient characteristics of IDC (18 male, 5 female; mean age 51 +/- 13 years [range: 23-72]; Mg group), who received oral magnesium supplements (15 mmol/day). All patients received oral ACE inhibitors and 22 were receiving digitalis and diuretics. A control group of 27 patients, matched for age, sex, symptoms, and additional treatment (22 male, 5 female; mean age 52 +/- 13 years [range 22-71]) were not given oral magnesium supplements. All these patients also received oral ACE inhibitors, 25 were receiving digitalis, and 23 were receiving diuretics. Mean serum magnesium concentration (total serum Mg) in the Mg group was 0.83 +/- 0.06 mmol/litre [mean +/- SD, range 0.69-0.99], while in the control group it was 0.83 +/- 0.07 mmol/litre [range 0.70-0.96], P = NS. Left ventricular ejection fraction (LV-EF) improved from 32 +/- 11 per cent [range 13-51] to 42 +/- 14 per cent [range 15-66] in the Mg group and from 30 +/- 13 per cent [range 10-52] to 42 +/- 11 per cent [range: 25-64] in the control group. We found that physiological oral Mg supplements did not influence serum magnesium, LV-EF, or prognosis. Furthermore, we found that 56 per cent of all patients improved when subjected to strict guidance and therapy with ACE inhibitors, digitalis, and diuretics.

Adult↗
PubMed1997

Bioavailability and pharmacokinetics of magnesium after magnesium fumarate administration in humans.

Bioavibility and pharmacokinetics of magnesium after magnesium fumarate administration in humans. The volunteers were given a single oral dose of 530 mg of magnesium on an empty stomach. The preparation was a magnesium fumarate tablet. The simplest formule to describe the course of blood magnesium concentration changes was a two exponential equation for an open monocompartmental model.

Adult↗
PubMed1994

Normal red cell magnesium concentrations and magnesium loading tests in patients with chronic fatigue syndrome.

Red blood cell magnesium concentrations were measured in samples from 89 patients who fulfilled the diagnostic criteria for chronic fatigue syndrome and the results compared to those found in an age and sex matched group selected from the normal population. No significant difference was found. Six patients were further investigated using a magnesium loading test to determine if there was any evidence of magnesium deficiency associated with this disorder. None was found. There is therefore no indication for the use of magnesium therapy in the management of this condition.

Adult↗
PubMed1995

Response of magnesium-deficient saplings in a young, open stand of Picea abies (L.) Karst. to elevated soil magnesium, nitrogen and carbon.

A decline in a Picea abies L. (Karst.) stand in the Fichtelgebirge, NE-Bavaria, FRG has been attributed to a nutritional disharmony-a seasonal imbalance between a high supply of nitrogen, caused by high nitrogen deposition, and a low supply of soil magnesium, caused by soil acidification (Oren et al., 1988a). The nutritional disharmony hypothesis was tested on ten-year-old P. abies saplings in an adjacent stand growing on identical soil. The supply rate of magnesium relative to nitrogen was continuously increased or decreased during three successive growing seasons. Increasing the nitrogen or carbon supply resulted in a small increase in foliar nitrogen concentrations. Magnesium or carbon addition slightly raised the concentration of magnesium in the foliage. Reduction in crown leaf-area did not result in any appreciable changes in nutrient concentrations. Increased N supply decreased foliar Mg concentrations. In spite of the changes in the nutritional status of the needles, gas-exchange rates, pigment concentrations, needle characteristics and growth of twigs and stems did not differ among treatments. It appears that the growth of saplings was unimpaired at the foliar magnesium concentration at which the growth of adjacent mature trees was reduced. Moreover, it was not possible to promote nutritional disharmony in the saplings, including those receiving three times the annual nitrogen input. The study demonstrates that in young, relatively open stands of P. abies, much of the deposited nitrogen is not absorbed by the roots of saplings. Thus, the conceptual model of nutritional disharmony cannot explain forest decline if nitrogen uptake does not increase with deposition. Identifying the processes which control the uptake relative to the supply of all nutrients, and quantifying the rates of nutrient uptake are essential steps in using the conceptual model to explain specific decline symptoms.

Journal Article↗
PubMed2005

Final report of the safety assessment of L-Ascorbic Acid, Calcium Ascorbate, Magnesium Ascorbate, Magnesium Ascorbyl Phosphate, Sodium Ascorbate, and Sodium Ascorbyl Phosphate as used in cosmetics.

L-Ascorbic Acid, Calcium Ascorbate, Magnesium Ascorbate, Magnesium Ascorbyl Phosphate, Sodium Ascorbate, and Sodium Ascorbyl Phosphate function in cosmetic formulations primarily as antioxidants. Ascorbic Acid is commonly called Vitamin C. Ascorbic Acid is used as an antioxidant and pH adjuster in a large variety of cosmetic formulations, over 3/4 of which were hair dyes and colors at concentrations between 0.3% and 0.6%. For other uses, the reported concentrations were either very low (<0.01%) or in the 5% to 10% range. Calcium Ascorbate and Magnesium Ascorbate are described as antioxidants and skin conditioning agents--miscellaneous for use in cosmetics, but are not currently used. Sodium Ascorbyl Phosphate functions as an antioxidant in cosmetic products and is used at concentrations ranging from 0.01% to 3%. Magnesium Ascorbyl Phosphate functions as an antioxidant in cosmetics and was reported being used at concentrations from 0.001% to 3%. Sodium Ascorbate also functions as an antioxidant in cosmetics at concentrations from 0.0003% to 0.3%. Related ingredients (Ascorbyl Palmitate, Ascorbyl Dipalmitate, Ascorbyl Stearate, Erythorbic Acid, and Sodium Erythorbate) have been previously reviewed by the Cosmetic Ingredient Review (CIR) Expert Panel and found "to be safe for use as cosmetic ingredients in the present practices of good use." Ascorbic Acid is a generally recognized as safe (GRAS) substance for use as a chemical preservative in foods and as a nutrient and/or dietary supplement. Calcium Ascorbate and Sodium Ascorbate are listed as GRAS substances for use as chemical preservatives. L-Ascorbic Acid is readily and reversibly oxidized to L-dehydroascorbic acid and both forms exist in equilibrium in the body. Permeation rates of Ascorbic Acid through whole and stripped mouse skin were 3.43 +/- 0.74 microg/cm(2)/h and 33.2 +/- 5.2 microg/cm(2)/h. Acute oral and parenteral studies in mice, rats, rabbits, guinea pigs, dogs, and cats demonstrated little toxicity. Ascorbic Acid and Sodium Ascorbate acted as a nitrosation inhibitor in several food and cosmetic product studies. No compound-related clinical signs or gross or microscopic pathological effects were observed in either mice, rats, or guinea pigs in short-term studies. Male guinea pigs fed a control basal diet and given up to 250 mg Ascorbic Acid orally for 20 weeks had similar hemoglobin, blood glucose, serum iron, liver iron, and liver glycogen levels compared to control values. Male and female F344/N rats and B6C3F(1) mice were fed diets containing up to 100,000 ppm Ascorbic Acid for 13 weeks with little toxicity. Chronic Ascorbic Acid feeding studies showed toxic effects at dosages above 25 mg/kg body weight (bw) in rats and guinea pigs. Groups of male and female rats given daily doses up to 2000 mg/kg bw Ascorbic Acid for 2 years had no macro- or microscopically detectable toxic lesions. Mice given Ascorbic Acid subcutaneous and intravenous daily doses (500 to 1000 mg/kg bw) for 7 days had no changes in appetite, weight gain, and general behavior; and histological examination of various organs showed no changes. Ascorbic Acid was a photoprotectant when applied to mice and pig skin before exposure to ultraviolet (UV) radiation. The inhibition of UV-induced suppression of contact hypersensitivity was also noted. Magnesium Ascorbyl Phosphate administration immediately after exposure in hairless mice significantly delayed skin tumor formation and hyperplasia induced by chronic exposure to UV radiation. Pregnant mice and rats were given daily oral doses of Ascorbic Acid up to 1000 mg/kg bw with no indications of adult-toxic, teratogenic, or fetotoxic effects. Ascorbic Acid and Sodium Ascorbate were not genotoxic in several bacterial and mammalian test systems, consistent with the antioxidant properties of these chemicals. In the presence of certain enzyme systems or metal ions, evidence of genotoxicity was seen. The National Toxicology Program (NTP) conducted a 2-year oral carcinogenesis bioassay of Ascorbic Acid (25,000 and 50,000 ppm) in F344/N rats and B6C3F(1) mice. Ascorbic Acid was not carcinogenic in either sex of both rats and mice. Inhibition of carcinogenesis and tumor growth related to Ascorbic Acid's antioxidant properties has been reported. Sodium Ascorbate has been shown to promote the development of urinary carcinomas in two-stage carcinogenesis studies. Dermal application of Ascorbic Acid to patients with radiation dermatitis and burn victims had no adverse effects. Ascorbic Acid was a photoprotectant in clinical human UV studies at doses well above the minimal erythema dose (MED). An opaque cream containing 5% Ascorbic Acid did not induce dermal sensitization in 103 human subjects. A product containing 10% Ascorbic Acid was nonirritant in a 4-day minicumulative patch assay on human skin and a facial treatment containing 10% Ascorbic Acid was not a contact sensitizer in a maximization assay on 26 humans. Because of the structural and functional similarities of these ingredients, the Panel believes that the data on one ingredient can be extrapolated to all of them. The Expert Panel attributed the finding that Ascorbic Acid was genotoxic in these few assay systems due to the presence of other chemicals, e.g., metals, or certain enzyme systems, which effectively convert Ascorbic Acid's antioxidant action to that of a pro-oxidant. When Ascorbic Acid acts as an antioxidant, the Panel concluded that Ascorbic Acid is not genotoxic. Supporting this view were the carcinogenicity studies conducted by the NTP, which demonstrated no evidence of carcinogenicity. Ascorbic Acid was found to effectively inhibit nitrosamine yield in several test systems. The Panel did review studies in which Sodium Ascorbate acted as a tumor promoter in animals. These results were considered to be related to the concentration of sodium ions and the pH of urine in the test animals. Similar effects were seen with sodium bicarbonate. Because of the concern that certain metal ions may combine with these ingredients to produce pro-oxidant activity, the Panel cautioned formulators to be certain that these ingredients are acting as antioxidants in cosmetic formulations. The Panel believed that the clinical experience in which Ascorbic Acid was used on damaged skin with no adverse effects and the repeat-insult patch test (RIPT) using 5% Ascorbic Acid with negative results supports the finding that this group of ingredients does not present a risk of skin sensitization. These data coupled with an absence of reports in the clinical literature of Ascorbic Acid sensitization strongly support the safety of these ingredients.

Administration, Oral↗
PubMed1997

Antiarrhythmic and Arrhythmogenic Actions of Varying Levels of Extracellular Magnesium: Possible Cellular Basis for the Differences in the Efficacy of magnesium and Lidocaine in Torsade de Pointes.

BACKGROUND: In recent years, there has been an increasing use of antiarrhythmic drugs that act predominantly by prolonging myocardial repolarization. An inevitable electrophysiologic consequence of these drugs is the development of torsade de pointes as a proarrhythmic reaction. Both intravenous lidocaine and magnesium sulphate have been used in the acute control of such a proarrhythmia. Their electrophysiologic mechanisms in this setting are not well defined. METHODS AND RESULTS: Using the standard microelectrode techniques, the effects of magnesium (Mg) and lidocaine on action potential duration (APD), and on barium-induced spontaneous action potentials, were studied in canine Purkinje fiber preparations. The objective was to clarify the direct and indirect effects of magnesium on triggered activities due to early afterdepolarizations. Superfusion in media with 0.1 mM Mg and 2.5 mM K produced more pronounced increases in APD measured at -20mV repolarization time [APD(20)] than those in a solution with 5 mM K. This effect was further enhanced at lower stimulation frequencies. The striking prolongation of APD(20) by solutions with low potassium concentrations diminished as the Mg concentration was increased. In solutions with 2.5 mM K, Mg produced concentration-dependent decreases in APD(20). This effect was greater at lower stimulation frequencies. Lidocaine at 4.0 x 10(_5) M produced a marked shortening of the APD in the entire firing frequency of the abnormal automaticity in a concentration-dependent manner. With 10 mM Mg, such action potentials appeared only sporadically. Magnesium also decreased the amplitude and the maximum upstroke velocity of these action potentials. In contrast, lidocaine at 4.0 x 10(-5) M exhibited no significant effects on action potentials due to barium-induced abnormal automaticity, or on additional depolarizations developing from the repolarization phase of these action potentials. CONCLUSIONS: The data indicate that (i) hypomagnesemia may be arrhythmogenic when combined with hypokalemia and bradycardia leading to a prolongation of the plateau phase of the action potential, (ii) magnesium administration may suppress triggered activities mainly by a direct inhibition of the development of triggered potentials, and (iii) lidocaine may suppress triggered potentials only indirectly by preventing the development of early afterdepolarizations due to the shortening effect on the APD. These findings are consistent with the clinical observation of a high incidence of torsade de pointes in the setting of hypokalemia and hypomagnesemia introduced by a chronic diuretic therapy. They are also consistent with the marked effectiveness of intravenous Mg relative to the inconsistent clinical effects of lidocaine in controlling torsade de pointes.

Journal Article↗
PubMed2002

Serum ionized magnesium levels and serum ionized calcium/ionized magnesium ratios in women with menstrual migraine.

OBJECTIVE: It has been suggested that magnesium deficiency may play an important role in menstrual migraine and that the serum ionized calcium (ICa2+)/ionized magnesium (IMg2+) ratio is important in migraine headache. Studies were designed to test these hypotheses. DESIGN: We prospectively evaluated 270 women seen at a headache clinic and in 61 women with menstrual migraine measured IMg2+, total magnesium, and ICa2+ levels so as to calculate the ICa2+/IMg2+ ratio. RESULTS: The incidences of IMg2+ deficiency were 45% during menstrual attacks, 15% during nonmenstrual attacks, 14% during menstruation without a migraine, and 15% between menstruations and between migraine attacks. The serum ICa2+ levels were within our reference range, but the ICa2+/IMg2+ ratio was elevated (P<.01) in menstrual migraine. CONCLUSIONS: The high incidence of IMg2+ deficiency and the elevated ICa2+/IMg2+ ratio during menstrual migraine confirm previous suggestions of a possible role for magnesium deficiency in the development of menstrual migraine.

Calcium↗
PubMed2000

Intralymphocyte free magnesium in patients with primary aldosteronism: aldosterone and lymphocyte magnesium homeostasis.

It is known that hyperaldosteronism has been associated with magnesium deficiency, yet there are no data on the intracellular concentration of ionized magnesium ([Mg(2+)(i)]) in subjects with primary aldosteronism (PA). We measured intralymphocyte free magnesium ([Mg(2+)(i)]) and intralymphocyte free calcium ([Ca(2+)(i)]) in 16 patients with PA and 26 normotensive control subjects (NCs). [Mg(2+)(i)] and [Ca(2+)(i)] were also measured in blood lymphocytes incubated in vitro with aldosterone, according to a fluorimetric method. In subjects with PA, [Mg(2+)(i)] was significantly lower than that in NCs (mean+/-SD; PA 203+/-56 micromol/L, NCs 291+/-43 micromol/L, 95% confidence interval 57 to 119, P=0.001). In the patients, [Ca(2+)(i)] did not prove to be statistically different from that of NCs (mean+/-SD; PA 47.2+/-10.6 nmol/L, NCs 53.2+/-11 nmol/L). The lymphocytes exposed to the action of aldosterone showed a significant reduction in [Mg(2+)(i)] (n=15, NCs 271+/-28 micromol/L, aldosterone treatment 188+/-39 micromol/L, P=0.001, 95% confidence interval 57 to 108). The dose-effect curve of aldosterone on [Mg(2+)(i)] showed an EC(50) value of approximately 0.5 to 1 nmol/L aldosterone. The reduction in [Mg(2+)(i)] mediated by aldosterone is antagonized by the receptor inhibitor of aldosterone; it is inhibited by inhibitors of protein synthesis and is not measurable when the lymphocytes are incubated in an Na(+)-free medium. The data are consistent with the hypothesis that aldosterone affects the cellular homeostasis of magnesium, probably through modification of the activity of the Na(+)-Mg(2+) antiporter.

Adult↗
PubMed1995

Serum magnesium levels during magnesium sulfate tocolysis in high-order multiple gestations.

The objective of this study was to determine the serum levels of magnesium associated with various intravenous infusion rates of magnesium sulfate (MgSO4) in high-order multiple gestations. A retrospective review of 12 triplet and 4 quadruplet pregnancies cared for in Phoenix from August 1988 to January 1992 was performed. The mothers received MgSO4 for tocolysis of preterm labor. Serum magnesium levels were drawn to help manage patients with symptoms of an excessive magnesium level or an inadequate tocolytic effect. The results are presented for triplets and quadruplets with and without pregnancy-induced hypertension (PIH). The serum levels of Mg++ in triplets and quadruplets were similar to those in singleton pregnancies described in the literature. Higher serum levels of Mg++(7.0-7.5 mg/dL) seemed to be necessary for successful tocolysis. Serum levels of Mg++ in patients with underlying PIH were significantly higher at the same intravenous infusion rate. MgSO4 may need to be administered at infusion rates of 4-5 g/h to achieve therapeutic levels in women with triplets and quadruplets. PIH should require lower infusion rates to achieve therapeutic serum levels of Mg++.

Female↗