Magnesium Deficiency and Excess

Rude, Robert K.; Singer, Frederick R.

doi:10.1146/annurev.me.32.020181.001333

Cited by 192 publications

(69 citation statements)

References 60 publications

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“…Furthermore, Mg 2 + concentrations lower than 0. 4 mM can be measured in various pathophysiological states (Rude and Singer, 1981;Altura and Altura, 1984;Scully, 1986).…”

Section: Discussionmentioning

confidence: 99%

Contractile and Endothelium-Dependent Dilatory Responses of Cerebral Arteries at Various Extracellular Magnesium Concentrations

Faragó

Szabó

Dóra

et al. 1991

J Cereb Blood Flow Metab

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Summary:To clarify the effect of extracellular magne sium (Mg2+) on the vascular reactivity of feline isolated middle cerebral arteries, the effects of slight alterations in the Mg2 + concentration on the contractile and endothe lium-dependent dilatory responses were investigated in vitro. The contractions, induced by 1O-8_IO-s M norepi nephrine, were significantly potentiated at low Mg2 + (0,8 mM v. the normal, 1.2 mM). High (1.6 and 2.0 mM) Mg2 + exhibited an inhibitory effect on the contractile re sponses, No significant changes, however, in the EC so values for norepinephrine were found. The endothelium dependent relaxations induced by 1O-8_10-s M acetyl choline were inhibited by high (1.6 and 2.0 mM) Mg2+. Lowering of the Mg2+ concentration to 0.8 mM or total withdrawal of this ion from the medium failed to alter the dilatory potency of acetylcholine. The changes in the dilDuring the past decade, a considerable amount of data has been generated concerning the effect of extracellular magnesium ions (Mg2 + ) on vascular smooth muscle tone and reactivity. Acute with drawal of Mg2 + elevates the basal tone of the arter ies, and contractile responses to various agonists are enhanced in Mg2+ -deficient solutions. Eleva tion of Mg2+ , however, relaxes the smooth muscle and attenuates vasoconstriction (see Altura and Al tura, 1981,1984,1985. Abbreviations used: ECso, 50% effective concentration; EDRF, endothelium-derived relaxing factor. From the original observations of Furchgott and ------------ 161atory responses also shifted the ECso values for acetyl choline to the right. The present results show that the contractile responses of the cerebral arteries are ex tremely susceptible to the changes of Mg2 + concentra tions. In response to contractile and endothelium dependent dilatory agonists, Mg2+ probably affects both the calcium influx into the endothelial and smooth muscle cells as well as the binding of acetylcholine to its endo thelial receptor. Since Mg2 + deficiency might facilitate the contractile but not the endothelium-dependent relax ant responses, the present study supports a role for Mg2 + deficiency in the development of the cerebral vasospasm.

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“…Furthermore, Mg 2 + concentrations lower than 0. 4 mM can be measured in various pathophysiological states (Rude and Singer, 1981;Altura and Altura, 1984;Scully, 1986).…”

Section: Discussionmentioning

confidence: 99%

Contractile and Endothelium-Dependent Dilatory Responses of Cerebral Arteries at Various Extracellular Magnesium Concentrations

Faragó

Szabó

Dóra

et al. 1991

J Cereb Blood Flow Metab

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“…The clinical syndrome of magnesium deficiency in man includes fatigue, depression, jerky and weak muscles, ataxia, athetoid movements, cardiac arrhythmia's and, if severe, convulsions [127][128][129][130] . The occurrence of carpopedal spasm, positive Chvostek and Trousseau's signs generally occur if there is a concomitant hypocalcaemia [128,129,131] . Low serum magnesium levels are more common in patients with a jejunostomy (70%) than patients with a retained colon (40%) [25] .…”

Section: Magnesium Depletionmentioning

confidence: 99%

Management of patients with a short bowel

Nightingale

1999

Nutrition

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“…Chronic magnesium (Mg) deficiency would result in hypocalcemia [1,2], because of the impairment of PTH secretion [3][4][5][6][7] and/ or resistance of target organ to PTH action [4,6,8]. Previous studies have demonstrated that serum PTH concentration was suppressed in patients with hypomagnesemia [4,5], and Mg substitution therapy enhanced PTH secretion and reversed PTH target-organ resistance, and thus serum calcium concentration returned to normal within several days [4,7].…”

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confidence: 99%

A Case of Magnesium Deficiency Associated with Insufficient Parathyroid Hormone Action and Severe Osteoporosis

et al. 2007

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Abstract. The relationship between osteoporosis and magnesium (Mg) deficiency is still controversial. Here we report a case of an 82-year-old woman with a giant adenomatous goiter and severe osteoporosis with multiple vertebral fractures, whose clinical course indicated that her osteoporosis was probably due to Mg deficiency. She visited our hospital for treatments of tetany. Laboratory data showed the existence of hypomagnesemia, hypocalcemia, hypokalemia, vitamin D deficiency, and slightly elevated intact PTH. Intravenous administration of Mg not only improved these electrolyte abnormalities but also increased serum levels of intact PTH, bone formation markers, 1,25-dihydroxyvitamin D, as well as bone resorption markers in the urine, and lowered urinary phosphate reabsorption. Hypomagnesemia on admission seemed to arise from long-lasting poor food intake and malnutrition, because it improved after the disappearance of dysphagia with a goiter resection. After the operation, BMD values at the lumbar spine and femoral neck obviously increased during 6 months of Mg supplementation without any specific therapies for osteoporosis. Mg deficiency in this case seemed to cause impaired secretion of PTH from the parathyroid and the refractoriness of bone and kidney to the hormone, which led to the suppression of both bone remodeling and renal vitamin D production. These processes were probably linked to her severe osteoporosis, which was reversed by Mg supplementation. SERUM calcium levels are normally regulated within a relatively narrow range by the parathyroid gland through a negative feedback mechanism: Increased secretion of parathyroid hormone (PTH) by a fall in blood calcium levels enhances the mobilization of calcium, mainly by bone resorption, and then calcium levels are rapidly restored. Chronic magnesium (Mg) deficiency would result in hypocalcemia [1, 2], because of the impairment of PTH secretion [3][4][5][6][7] and/ or resistance of target organ to PTH action [4,6,8].Previous studies have demonstrated that serum PTH concentration was suppressed in patients with hypomagnesemia [4,5], and Mg substitution therapy enhanced PTH secretion and reversed PTH target-organ resistance, and thus serum calcium concentration returned to normal within several days [4,7]. In addition, Mg deficiency could inhibit the synthesis of 1,25-dihydroxy vitamin D (1,25(OH) 2 D) [9][10][11] as well as its action on bone [11]. Accumulating data have shown that a long-term Mg deficiency and resulting hypomagnesemia could cause osteoporosis and bone fractures through these dysfunctions of PTH and vitamin D action [12,[13][14][15][16][17][18][19]. However, other studies have shown no relationship between Mg deficiency and osteoporosis [20][21][22], and it still seems to be controversial whether or not Mg deficiency could cause osteoporosis. Here we report a patient with a giant adenomatous goiter and severe osteoporosis exhibiting hypomagnesemic hypocalcemia, whose osteoporosis was reversed by Mg supplementation with chronological improv...

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Magnesium Deficiency and Excess

Cited by 192 publications

References 60 publications

Contractile and Endothelium-Dependent Dilatory Responses of Cerebral Arteries at Various Extracellular Magnesium Concentrations

Contractile and Endothelium-Dependent Dilatory Responses of Cerebral Arteries at Various Extracellular Magnesium Concentrations

Management of patients with a short bowel

A Case of Magnesium Deficiency Associated with Insufficient Parathyroid Hormone Action and Severe Osteoporosis

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