Magnesium research最新文献

Dietary magnesium deficiency increases osteoclastic bone resorption and decreases osteoblastic bone formation. Increased bone resorption due to dietary magnesium deficiency can be explained by increased expression of the receptor activator of nuclear factor kB ligand. However, the detailed mechanisms underlying decreased bone formation remain unclear. Thus, in the present study, to determine the mechanism underlying decreased bone formation induced by dietary magnesium deficiency, we investigated the effects of short-term dietary magnesium deficiency on the mRNA expression of genes related to bone formation in rats. Male Wistar rats were fed a control or magnesium-deficient diet for eight days. The mRNA expression level of Runx2, Sp7, Bglap, Alpl, Col1a1, Igf1, and Bmp2 in the femur was significantly lower in magnesium-deficient rats than in control rats. These results suggest that short-term dietary magnesium deficiency decreases the gene expression of insulin-like growth factor-1 and bone morphogenetic protein 2, which, in turn, decreases osteoblastic bone formation through the downregulation of osteoblastogenesis-related gene expression.

The maintenance of various physiological cellular processes requires mineral magnesium (Mg). The purpose of the study was to determine a possible association between Mg level and vitamin D levels, bone mineral density (BMD), chronic diseases, and radiographic stage in individuals with knee osteoarthritis (OA). The study included 98 individuals (62 female and 36 male) who had been diagnosed with at least grade 1 knee OA. Age, sex, smoking, body mass index (BMI), family history of osteoporosis, menopausal status, duration of menopause, the presence of chronic diseases (hypertension, diabetes mellitus, hyperlipidaemia, coronary artery disease, hypothyroidism) and radiological stage of knee OA were gathered from all patients. Also, serum calcium, Mg, alkaline phosphatase, parathyroid hormone (PTH) and 25(OH)-vitamin D levels were recorded. Additionally, dual-energy X-ray absorptiometry (DEXA) was used to measure the BMD of the lumbar vertebrae (L1-L4) and femoral neck as well as anteroposterior radiography of the knee in all patients. T scores ≤-2.5 were accepted as evidence of osteoporosis. The mean age of the study population was 59.15 ± 10.58 years. The level of Mg significantly correlated with age, smoking, presence of chronic disease, duration of menopause, the level of vitamin D and PTH, and femoral neck T score (p<0.05). This study provides data supporting the relationship between magnesium levels and PTH and vitamin D levels, bone mineral density, and chronic disease. Future research is needed to examine the potential link between knee osteoarthritis and magnesium status.

Magnesium enhances the effects of neuromuscular blocking agents. However, there is a paucity of evidence demonstrating possible effects of magnesium on neostigmine-induced recovery from neuromuscular blockade with rocuronium. This study compared the profiles of recovery from neuromuscular blockade between groups treated with magnesium (Group M) and placebo controls (Group C). Sixty-four patients were randomly allocated to Group M or Group C. Patients in Group M received a loading dose of 50 mg/kg magnesium and continuous infusion of 15 mg/kg/hr. Patients in Group C received a comparable amount of saline. Rocuronium at 0.6 mg/kg was used for tracheal intubation and 0.1 mg/kg of rocuronium was additionally administered to maintain train-of-four (TOF) status of 2-3 during surgery. At the end of surgery, neostigmine (50 μg/kg) plus glycopyrrolate (10 μg/kg) were administered, and the recovery time for TOF ratios of 0.7, 0.8, and 0.9 was measured. The primary outcome was the time from neostigmine administration to recovery with a TOF ratio of 0.9. In addition, rocuronium onset time (time from administration of rocuronium to 95% suppression of the first TOF twitch response), additional requirements for rocuronium and spontaneous recovery period (the time from administration of rocuronium to reappearance of the first TOF twitch response) were also measured. Neostigmine-induced recovery time was comparable between Group M and Group C (10.6 ± 4.3 vs. 9.1 ± 5.0 min, respectively, p = 0.22). The rocuronium onset time was shorter in Group M, and the spontaneous recovery period was longer in Group M. The amount of additional rocuronium administered was 27% lower in Group M, but this difference was not significant. Magnesium was not shown to prolong neostigmine-induced recovery time from neuromuscular blockade with rocuronium, however, it enhanced the clinical effects of rocuronium.

According to epidemiological studies, constipation has a negative effect on life expectancy, necessitating appropriate treatment. According to the Pharmaceuticals and Medical Devices Agency (PMDA), patients who have been taking magnesium oxide (MgO) for constipation over a prolonged period, especially those with impaired renal function and older individuals, are at high risk of hypermagnesemia. Therefore, serum Mg levels, which are often not checked in clinical practice, should be monitored in these patients. Thus, to predict elevated serum Mg levels and prevent the development of hypermagnesemia, we aimed to identify the risk factors of hypermagnesemia, especially in the older population. Our study included patients who were prescribed MgO at our hospital between January 1, 2014, and March 31, 2016. Patients who did not meet the inclusion criteria were excluded and matched to adjust for background factors; finally, 35 patients in the hypermagnesemia arm and 140 patients in the non-hypermagnesemia arm were included in the analysis. Multivariate analysis identified estimated creatinine clearance (eCcr) ≤ 28.2 mL/min as a statistically significant risk factor. In addition, MgO dose ≥ 900 mg/day was identified as a risk factor for clinical consideration, although not statistically significant. Furthermore, the incidence of hypermagnesemia was shown to increase to 11.6% for those with MgO dose ≥ 900 mg/day, 27.0% for those with eCcr ≤ 28.2 mL/min, and 53.1% for those with both. Hypermagnesemia may occur in older patients with eCcr ≤ 28.2 mL/min who take more than 900 mg/day of MgO.

Severe hemodynamic instability is observed during portal vein de-clamping in the form of post-reperfusion syndrome in liver transplantation. The protective effect of magnesium on inflammation and ischemia-reperfusion injuries of various organs is evident, but its role in the prevention of post-reperfusion syndrome in liver transplantation is not clear. We investigated the effect of magnesium sulphate on the incidence of post-reperfusion syndrome during living donor liver transplantation. The secondary outcomes were the requirement of vasopressor boluses and levels of serum magnesium, lactate and serum C-reactive protein. Seventy living donor liver transplant recipients were randomized into a magnesium (M) group (n = 35) or normal saline (N) group (n = 35). The patients in group M received 35 mg/kg of magnesium sulphate, 30 minutes after the beginning of the anhepatic phase, and patients in group N received normal saline. The incidence of post-reperfusion syndrome in group M and group N was 34.29% and 40%, respectively, with no significant difference. The requirement for rescue vasopressor boluses and levels of C-reactive protein and lactate were also comparable between the two groups. However, the incidence of hypomagnesemia at the end of surgery was significantly higher in group N (37.1% vs. 14.28%, p = 0.027). Magnesium does not appear to prevent post-reperfusion syndrome. However, hypomagnesemia is more frequently seen during liver transplantation. Hence, serum magnesium should be routinely monitored and administered during liver transplantation.

Oxidative stress, arising from disrupted balance between reactive oxygen/nitrogen species (ROS/RNS) and antioxidant defences, has been implicated in the pathogenesis of stress-related disorders. There is a growing body of evidence that supports the relationship between the activity of the hypothalamic-pituitary-adrenal (HPA) stress system, oxidative stress and magnesium (Mg) homeostasis. The present study aimed to explore the gap in our current understanding of antigenotoxic and protective effects of Mg supplementation against excessive ROS production in male rats during chronic treatment with adrenocorticotropic hormone (ACTH). Our findings show that exposure to exogenous ACTH (10 μg/day, s.c., for 21 days), as one of the key mediators of the HPA axis and stress response, produced an increase in superoxide anion levels and a decrease in superoxide dismutase activity in plasma. We observed that Mg supplementation, starting seven days prior to ACTH treatment and lasting 28 days (300 mg/L of drinking water, per os), abolished these effects in experimental animals. Moreover, our study reveals that ACTH increased the susceptibility of peripheral blood lymphocytes to ex vivo H2O2-induced total and high-level oxidative DNA damage, while Mg completely reversed these effects. Collectively, these results highlight the promising role of Mg in stress-related conditions accompanied by increased oxidative stress in animals and support further investigation using human dietary trials.

Background: Hypomagnesemia is a common electrolyte abnormality in hospitalized patients. Prolonging the infusion rate of magnesium has been hypothesized to increase retention of magnesium, however, there is limited evidence to support prolonging the rate of infusion.

Aim: To compare the absolute change in serum magnesium levels from baseline to levels drawn within 24 hours after the end of infusion between two groups receiving standard or prolonged infusion.

Methods: This was a retrospective, observational cohort study comparing patients receiving magnesium infusion at a standard rate of 0.5 gm/h to those receiving magnesium infusion at a prolonged rate of 0.17 gm/h.

Results: Of a total of 276 patients, 138 were included in each group. No differences existed between the groups for any demographic variables (all p>0.05). The absolute change in serum magnesium level was 0.41 mg/dL versus 0.31 mg/dL in the standard and the prolonged infusion groups, respectively (p = 0.001). The length of stay after the initial magnesium dose was slightly longer with the prolonged infusion compared to the standard infusion, with a median of 2.9 days versus 3.6 days, respectively (p = 0.02). No differences existed between the groups for any secondary or safety outcomes (all p>0.05).

Conclusion: Hospitalized general patients did not benefit from the prolonged infusion of magnesium compared to standard infusion.

Introduction: Magnesium sulphate (MgSO4) is administered to pregnant women at risk of preterm labour and eclampsia. Since prolonged exposure to antenatal MgSO4 is considered to be a risk factor for infant skeletal demineralization, we evaluated infants exposed to antenatal MgSO4 for bone and mineral metabolism using their umbilical cord blood.

Materials and methods: The study population comprised 137 preterm infants. Forty-three infants were exposed (exposure group) and 94 infants were not exposed (control group) to antenatal MgSO4. Blood samples from the umbilical cords and infants were analysed with respect to mineral metabolism, intact parathyroid hormone (iPTH) level, and alkaline phosphatase (ALP) level. Correlation between the level of these parameters and the duration and dosage of MgSO4 was also examined.

Results: Preterm infants in the exposure group were antenatally exposed to MgSO4 for a median (IQR) period of 14 (5-34) days and a dosage of 447 (138-1118) g. Serum calcium levels were lower (8.8 vs 9.4 mg/dL, p<0.001) and ALP levels were higher (312 vs 196 U/L, p<0.001) in the exposure group. Serum calcium levels did not correlate with MgSO4 administration dosage and therapy duration, however, ALP levels correlated with the duration and total dosage of MgSO4 (Spearman's rank correlation r [95% confidence interval]: 0.55 [0.30-0.73], p <0.001 and 0.63 [0.40-0.78], p <0.001, respectively).

Conclusion: Prolonged periods and higher doses of antenatal MgSO4 exposure can cause in utero abnormal bone metabolism in preterm infants.