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Background: Magnesium is an essential intracellular cation. Magnesium deficiency is common in the general population and its prevalence among patients with cirrhosis is even higher. Correlation between serum levels and total body content is poor because most magnesium is intracellular. Minimal hepatic encephalopathy is a subclinical phase of hepatic encephalopathy with no overt symptoms. Cognitive exams can reveal minor changes in coordination, attention, and visuomotor function, whereas language and verbal intelligence are usually relatively spared., Objectives: To assess the correlation between intracellular and serum magnesium levels and minimal hepatic encephalopathy., Methods: Outpatients with a diagnosis of compensated liver cirrhosis were enrolled in this randomized, double-blinded study. Patients were recruited for the study from November 2013 to January 2014, and were randomly assigned to a control (placebo) or an interventional (treated with magnesium oxide) group. Serum and intracellular magnesium levels were measured at enrollment and at the end of the study. Cognitive function was assessed by a specialized occupational therapist., Results: Forty-two patients met the inclusion criteria, 29 of whom were included in this study. Among these, 83% had abnormal cognitive exam results compatible with minimal hepatic encephalopathy. While only 10% had hypomagnesemia, 33.3% had low levels of intracellular magnesium. Initial intracellular and serum magnesium levels positively correlated with cognitive performance., Conclusions: Magnesium deficiency is common among patients with compensated liver cirrhosis. We found an association between magnesium deficiency and impairment in several cognitive function tests. This finding suggests involvement of magnesium in the pathophysiology of minimal hepatic encephalopathy.

We sought to investigate whether magnesium oxide bound to soy protein (MGP) increases serum magnesium concentrations with less diarrhea compared to commonly prescribed magnesium salts. Subjects were switched to MGP at a near-equivalent daily elemental magnesium dose. Mean serum magnesium levels were compared. If magnesium levels remained <1.7 mg/dL after switching to MGP, subjects were enrolled into Part 2 and received a one-time MGP dose adjustment. The MGP daily dose was increased by 266 mg. For both parts 1 and 2, subjects recorded the number and quality of their stools to assess gastrointestinal (GI) tolerability of MGP. Twelve pediatric kidney transplant recipients completed Part 1. Mean serum magnesium levels increased from 1.61 (SD 0.1) on standard MG to 1.69 (SD 0.1); t(11) = 2.6, P = .02 on MGP. Five subjects completed Part 2, and all achieved serum magnesium ≥1.7 mg/dL (mean 1.75 mg/dL, SD 0.06; t(4) = 2.7, P = .06). Subjects reported the same number of, but looser bowel movements with MGP; however, individuals did not perceive intolerable GI symptoms with MGP therapy and all chose to remain on MGP at the end of the study. At an equivalent mg/kg/d dose of elemental magnesium, serum magnesium levels on MGP were significantly higher., (© 2018 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Post-transplantation hypomagnesemia is common and predicts diabetes. Magnesium improves glycemic control in diabetics and insulin sensitivity in insulin resistant subjects. We aimed to assess the effectiveness of oral magnesium for improving glycemic control and insulin sensitivity at 3 months post-transplantation. We conducted a single-center, open-label, randomized parallel group study. We included adults with serum magnesium <1.7 mg/dl within 2 weeks after kidney transplantation. We randomized participants to 450 mg magnesium oxide up to three times daily or no treatment. The primary endpoint was the mean difference in fasting glycemia. Secondary endpoints were the mean difference in area under the curve (AUC) of glucose during an oral glucose tolerance test and insulin resistance measured by Homeostasis Model of Assessment-Insulin Resistance (HOMA-IR). Analyses were on intention-to-treat basis. In patients randomized to magnesium oxide (N = 27) versus no treatment (N = 27), fasting glycemia on average was 11.5 mg/dl lower (95% CI 1.7 to 21.3; P = 0.02). There was no difference between the two groups neither for 2 h AUC, where the mean value was 1164 mg/dl/min (95% CI -1884 to 4284; P = 0.45) lower in the treatment group nor for HOMA-IR. Magnesium supplements modestly improved fasting glycemia without effect on insulin resistance. Higher baseline glycemia among patients in the control group may have driven the positive outcome (ClinicalTrials.gov number: NCT01889576)., (© 2014 Steunstichting ESOT.)

Background: Magnesium deficiency is associated with poor physical performance, but no trials are available on how magnesium supplementation affects elderly people's physical performance., Objective: The aim of our study was to investigate whether 12 wk of oral magnesium supplementation can improve physical performance in healthy elderly women., Design: In a parallel-group, randomized controlled trial, 139 healthy women (mean ± SD age: 71.5 ± 5.2 y) attending a mild fitness program were randomly allocated to a treatment group (300 mg Mg/d; n = 62) or a control group (no placebo or intervention; n = 77) by using a computer-generated randomization sequence, and researchers were blinded to their grouping. After assessment at baseline and again after 12 wk, the primary outcome was a change in the Short Physical Performance Battery (SPPB); secondary outcomes were changes in peak torque isometric and isokinetic strength of the lower limbs and handgrip strength., Results: A total of 124 participants allocated to the treatment (n = 53) or control (n = 71) group were considered in the final analysis. At baseline, the SPPB scores did not differ between the 2 groups. After 12 wk, the treated group had a significantly better total SPPB score (Δ = 0.41 ± 0.24 points; P = 0.03), chair stand times (Δ = -1.31 ± 0.33 s; P < 0.0001), and 4-m walking speeds (Δ = 0.14 ± 0.03 m/s; P = 0.006) than did the control group. These findings were more evident in participants with a magnesium dietary intake lower than the Recommended Dietary Allowance. No significant differences emerged for the secondary outcomes investigated, and no serious adverse effects were reported., Conclusions: Daily magnesium oxide supplementation for 12 wk seems to improve physical performance in healthy elderly women. These findings suggest a role for magnesium supplementation in preventing or delaying the age-related decline in physical performance., (© 2014 American Society for Nutrition.)

Five cows in a herd of 15 cattle that had just been turned out onto lush pasture after having over-wintered on poor quality hay died suddenly. Biochemical profiles collected from the cadavers revealed reduced serum levels of magnesium, urea, and beta-hydroxybutycate. Classical grass tetany (hypomagnesemia) was diagnosed on postmortem examination.

A female Thai baby born to non-consanguineous parents, presented with primary hypomagnesemia at 10 weeks of age, and suffered recurrent convulsions that responded to magnesium supplementation. She was found to have hypomagnesemia (Mg 0.35-1.02 mEq/L) and a low urinary magnesium excretion of less than 10 mg per day, or urinary Mg/Cr that ranged from 0.005-0.01 mg/mg. Intermittent hypomagnesemia and one episode of hypocalcemia with occasional convulsions developed, due to irregular consumption of oral magnesium sulfate, which had a bitter taste, caused frequent loose stools and black staining of the teeth. Better compliance after switching from magnesium sulfate to magnesium oxide resulted in an increased level of serum magnesium and the gradual disappearance of the black staining of the teeth and frequent loose stools. The patient required an oral elemental magnesium dosage of 15-30 mg/kg/day to maintain the serum magnesium level at between 1.02-1.33 mEq/L and keep her free from convulsions. The follow-up period was 7 years during which the patient showed normal physical growth and a mild degree of mental retardation.

Background: Hypomagnesemia has been associated with hypertension, abnormal glucose and lipid metabolism, and accelerated atherosclerosis in nontransplant patients., Methods: In this prospective short-term pilot study, 14 hypomagnesemic renal transplant recipients with stable renal function were evaluated monthly over a 6-month interval. The first 3 months was the baseline observation period. During the second 3 months, MgO2 was administered to normalize the serum Mg level. Glucose tolerance, lipid levels, blood pressure, weight, and routine chemistries were assessed before and after Mg replacement. All others medications were held constant during the 6-month study., Results: Serum Mg levels increased to normal range after MgO2 therapy, which was well tolerated. There were significant decreases in total cholesterol, low density lipoprotein, and total cholesterol/high density lipoprotein ratio after 3 months of MgO2 therapy. Only three patients had abnormal baseline glucose tolerance tests. All three patients showed improved glucose tolerance after MgO2, but this was not statistically significant., Conclusions: Mg repletion may be an important ancillary therapy in hypomagnesemic renal transplant patients with hyperlipidemia.

Isolated magnesium malabsorption is a rare disorder, which bas been described in no more than 30 patients worldwide. Patients with this disorder typically present with convulsion and diarrhea in early infancy. Hypomagnesemia and hypocalcemia were found in a 35-year-old man with muscle cramps, who bad been diagnosed as primary hypoparathyroidism. Oral magnesium therapy corrected the low serum calcium, magnesium and parathyroid hormone levels. We report an atypical case of isolated magnesium malabsorption in an adult.

Seven patients with severe neuromuscular symptoms due to hypomagnesaemia together with hypocalcaemia following extensive resection of the small bowel were treated orally with 1 alpha-hydroxylated metabolites of vitamin D and magnesium oxide. There was a rapid response in both plasma calcium and magnesium concentrations. The mean plasma magnesium rose from 0.24 to 0.45 mmol/l with the vitamin D metabolites alone and to 0.81 mmol/l when magnesium oxide was added. The plasma calcium rose from 1.78 to 2.21 mmol/l on vitamin D alone and then remained within the normal range. This was accompanied by a rapid resolution of the neuromuscular symptoms. Such oral treatment is both acceptable to the patient and effective both for acute symptoms and in the long term to maintain plasma magnesium concentrations.

In 78 patients with hypomagnesemia in urolithiasis the clinical course of disease was established in relation to therapy and dynamics of changes of serum magnesium levels. Almost 70% of patients had multiple, bilateral or recurrent nephrolithiasis or nephrocalcinosis. 70% of patients had Ca-oxalate stones or bilateral nephrocalcinosis. In 52% of patients a long-term magnesium supplementation was necessary. Significant progress of nephrolithiasis and nephrocalcinosis was observed in 80% of patients with permanent hypomagnesemia and in 4% of patients with normalization of serum magnesium level. Three of 15 patients with hypomagnesemia and progress of disease were transplanted a kidney and two were treated by hemodialysis. All five patients with renal failure had bilateral nephrocalcinosis, in three of them familiar occurrence of nephrolithiasis and hypomagnesemia was found.

A field experiment was undertaken in northern Ontario in order to assess the magnesium status of beef cattle raised in the area. Magnesium status was assessed using several criteria including blood and urine magnesium levels, and bone biopsy samples. Eighteen groups each containing four pregnant Shorthorn beef cows were used. Each of the following three mineral feeds were offered to six groups throughout the experiment: a mineral feed without magnesium, a mineral feed containing 8% magnesium in the form of magnesium oxide and the third containing sequestered magnesium with a magnesium level of about a tenth of that in the mineral feed containing magnesium oxide. During the winter, when the cows were housed indoors, they were fed grass silage. Six groups, two of each mineral feed, remained indoors throughout the summer. The other 12 groups were turned out to pasture on May 25 and continued receiving the appropriate mineral feed. There were no differences in serum magnesium owing to magnesium-supplementation treatments observed at any time during any experiment. Serum magnesium levels fell drastically in all groups before the cows were released to pasture, implying that the hypomagnesaemic condition was attributable to the stress of yarding. The rate of recovery from hypomagnesaemia was slower in the cows released to pasture than in those kept indoors. Urine samples from cows returned to the pasture were indicative of low magnesium status. At the end of the experiment, the magnesium levels in the bones of the housed animals were higher than for those on pasture. In spite of severe cases of hypomagnesaemia, no clinical signs of this metabolic condition were observed.

A 51-year-old man who had a past history of gastric resection for medically uncontrollable gastric ulcer has loss of appetite that recurs periodically. And he has frequently presented spontaneous angina early in the morning since 1984. He was diagnosed as having variant angina by the documentation of typical ST elevation during anginal attack and also by showing coronary artery spasm (#2 and #12) during hyperventilation on coronary arteriography. A large quantity of calcium blocking agents and nitrates could not improve his symptoms. Lack of intracellular magnesium by loss of appetite was suspected from a daily excretion of urine magnesium (5.3 mEq) and magnesium tolerance test (56.7%). To confirm the effect of magnesium administration, the second coronary arteriography was performed. After magnesium sulphate (80 mEq, hourly) was injected, coronary artery spasm could not be induced by ergonovine. And orally magnesium oxide, calcium blocking agents and nitrates were started. Anginal attack disappeared with increasing urine magnesium.