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Context: Low magnesium levels, which are common in people with type 2 diabetes, are associated with increased levels of proinflammatory molecules. It is unknown whether magnesium supplementation decreases this low-grade inflammation in people with type 2 diabetes., Objective: We performed multidimensional immunophenotyping to better understand the effect of magnesium supplementation on the immune system of people with type 2 diabetes and low magnesium levels., Methods: Using a randomized, double-blind, placebo-controlled, 2-period, crossover study, we compared the effect of magnesium supplementation (15 mmol/day) with placebo on the immunophenotype, including whole blood immune cell counts, T-cell and CD14+ monocyte function after ex vivo stimulation, and the circulating inflammatory proteome., Results: We included 12 adults with insulin-treated type 2 diabetes (7 males, mean ± SD age 67 ± 7 years, body mass index 31 ± 5 kg/m2, HbA1c 7.5 ± 0.9%) and low magnesium levels (0.73 ± 0.05 mmol/L). Magnesium treatment significantly increased serum magnesium and urinary magnesium excretion compared with placebo. Interferon-γ production from phorbol myristate acetate/ionomycin stimulated CD8+ T-cells and T-helper 1 cells, as well as interleukin (IL) 4/IL5/IL13 production from T-helper 2 cells was lower after treatment with magnesium compared with placebo. Magnesium supplementation did not affect immune cell numbers, ex vivo monocyte function, and circulating inflammatory proteins, although we found a tendency for lower high sensitivity C-reactive protein levels after magnesium supplementation compared with placebo., Conclusion: In conclusion, magnesium supplementation modulates the function of CD4+ and CD8+ T-cells in people with type 2 diabetes and low serum magnesium levels., (© The Author(s) 2024. Published by Oxford University Press on behalf of the Endocrine Society.)

This systematic review evaluates the hypothesis that optimal serum magnesium levels may enhance remission rates in Crohn's disease (CD) and considers whether magnesium supplementation could be beneficial in CD management. This review aims to synthesize available evidence concerning the impact of serum magnesium on disease remission in CD, and to analyze the effectiveness and mechanistic roles of magnesium supplementation. Adhering to the PRISMA guidelines, we searched PubMed, Web of Science, and Scopus up to January 2024 using MeSH terms and free-text queries related to CD and magnesium. The inclusion criteria were studies that investigated serum magnesium levels, effects of supplementation, and the inflammatory mechanisms in CD remission. From the 525 records identified, eight studies met the inclusion criteria after the removal of duplicates and irrelevant records. These studies, conducted between 1998 and 2023, involved a cumulative sample of 453 patients and 292 controls. Key findings include significantly lower serum magnesium levels in CD patients (0.79 ± 0.09 mmol/L) compared to controls (0.82 ± 0.06 mmol/L), with up to 50% prevalence of hypomagnesemia in CD patients observed in one study. Notably, CD patients, particularly men, exhibited lower magnesium intake (men: 276.4 mg/day; women: 198.2 mg/day). Additionally, low magnesium levels correlated with increased sleep latency (95% CI -0.65 to -0.102; p = 0.011) and decreased sleep duration (95% CI -0.613 to -0.041; p = 0.028). Another key finding was the significant association between low serum magnesium levels and elevated CRP levels as an indicator of CD disease activity. The findings support the hypothesis that serum magnesium levels are significantly lower in CD patients compared to healthy controls and suggest that magnesium supplementation could improve CD management by enhancing remission rates and sleep quality. However, more rigorous, evidence-based research is necessary to define specific supplementation protocols and to fully elucidate the role of magnesium in CD pathophysiology.

Magnesium (Mg 2+ ), also known as "the forgotten ion," is the second most abundant intracellular cation and is essential in a broad range of intracellular physiological and biochemical reactions. Its deficiency, hypomagnesemia (Mg 2+ <1.8mg/dL), is a prevalent condition and routinely poses challenges in its management in clinical practice. Sodium/glucose cotransporter 2 (SGLT2) inhibitors have emerged as a new class of drugs with treating hypomagnesemia as their unique extraglycemic benefit. The beneficial effect of SGLT2 inhibitors on magnesium balance in patients with diabetes with or without hypomagnesemia has been noted as a class effect in recent meta-analysis data from randomized clinical trials. Some reports have demonstrated their role in treating refractory hypomagnesemia in patients with or without diabetes. Moreover, studies on animal models have attempted to illustrate the effect of SGLT2 inhibitors on Mg 2+ homeostasis. In this review, we discuss the current evidence and possible pathophysiological mechanisms, and we provide directions for further research. We conclude by suggesting the effect of SGLT2 inhibitors on Mg 2+ homeostasis is a class effect, with certain patients gaining significant benefits. Further studies are needed to examine whether SGLT2 inhibitors can become a desperately needed novel class of medicines in treating hypomagnesemia., (Copyright © 2024 National Kidney Foundation, Inc. All rights reserved.)

Increasing evidence has suggested a clinical relevance of magnesium in the context of vascular calcification and mortality among patients with CKD. Hypomagnesemia is not rare among non-dialysis CKD patients despite their decreased glomerular filtration rates; the prevalence rate was about 15% even in CKD stages G4 and G5. Among several potential causes of hypomagnesemia, tubular dysfunction/interstitial fibrosis may play a pivotal role in the development of hypomagnesemia in CKD, which impairs tubular magnesium reabsorption. Magnesium deficiency may, in turn, be involved in the progression of CKD. An in vitro study has revealed that magnesium deficiency aggravates tubular cell death and inflammation induced by phosphate load. In a cohort study of patients with CKD, low-serum magnesium levels enhanced the risk of end-stage kidney disease related to high-serum phosphate levels, suggesting a close relationship between magnesium deficiency and phosphate toxicity. More importantly, magnesium has a potent capacity to inhibit the calcification of vascular smooth muscle cells induced by phosphate. A randomized trial has shown the efficacy of oral magnesium oxide in retarding the progression of coronary artery calcification among non-dialysis CKD patients. Thus, magnesium might provide better cardiovascular prognosis; indeed, hemodialysis patients with mild hypermagnesemia exhibited the lowest mortality rate. Further randomized trials are needed to assess the impact of magnesium in terms of hard clinical outcomes among CKD patients., (© 2022. The Author(s).)

So far, no coherent and convincing theory has been developed to fully explain the pathogenesis of migraine, although many researchers and experts emphasize its association with spreading cortical depression, oxidative stress, vascular changes, nervous excitement, neurotransmitter release, and electrolyte disturbances. The contribution of magnesium deficiency to the induction of cortical depression or abnormal glutamatergic neurotransmission is a likely mechanism of the magnesium-migraine relationship. Hence, there is interest in various methods of assessing magnesium ion deficiency and attempts to study the relationship of its intra- and extracellular levels with the induction of migraine attacks. At the same time, many clinicians believe that magnesium supplementation in the right dose and form can be a treatment to prevent migraine attacks, especially in those patients who have identified contraindications to standard medications or their different preferences. However, there are no reliable publications confirming the role of magnesium deficiency in the diet as a factor causing migraine attacks. It also seems interesting to deepen the research on the administration of high doses of magnesium intravenously during migraine attacks. The aim of the study was to discuss the probable mechanisms of correlation of magnesium deficiency with migraine, as well as to present the current clinical proposals for the use of various magnesium preparations in complementary or substitute pharmacotherapy of migraine. The summary of the results of research and clinical observations to date gives hope of finding a trigger for migraine attacks (especially migraine with aura), which may turn out to be easy to diagnose and eliminate with pharmacological and dietary supplementation.

Supplementation of various substances (metabolites, microelements, vitamins) is sometimes recommended without sufficient indications. To decide whether a supplementation is needed, the question should be answered whether there is a deficiency, and if there is, if it can be compensated by diet. Magnesium (Mg) deficiency has been associated with cardiovascular diseases, certain metabolic and neuropsychiatric disorders. Hypomagnesemia is above-average in alcoholism; however, alcoholics should not be a priori assumed to have Mg deficiency. Mild depletion does not necessarily require supplementation. The parenteral route is mandatory in severe Mg deficiency. Hypermagnesemia may result from excessive supplementation. Intravenous infusions of Mg-containing solutions have sometimes been used in alcoholics without sufficient indications. In conditions of suboptimal procedural quality assurance, endovascular and other invasive manipulations can lead to transmission of viral hepatitis. It has been suggested to include Mg in routine blood ionograms. The contents of Mg in different foodstuffs should be taken into account in patients at risk of Mg deficiency to better manage the diet.

Objective: Familial hypomagnesemia with secondary hypocalcemia (HSH) is an autosomal recessive disease caused by a mutation in the transient receptor potential melastatin 6 ( TRPM6 ) gene and is characterized by selective magnesium malabsorption. Affected cases are usually diagnosed during infancy and usually present with seizures due to hypocalcemia and hypomagnesemia. Irreversible neurological deficits and arrhythmias can be observed without appropriate treatment. The aim was to evaluate the long-term follow-up of patients with genetically confirmed HSH., Methods: A total of six patients with HSH, two of whom were siblings, were included. Age at diagnosis, clinical, laboratory and follow-up data on admission were recorded. All 39 exons of the TRPM6 gene and flanking exon-intron junctions from genomic DNA were amplified and sequenced in all cases., Results: The median (range) follow-up duration was 12.1 (7.6-21.7) years. All cases were diagnosed in infancy. Four different mutations, three of which had not been previously reported, were detected in the TRPM6 gene. Treatment compliance was good and there were no severe complications in the long-term follow-up of cases. However, mental retardation, specific learning difficulty and attention deficit/hyperactive disorder were observed as comorbidities., Conclusion: Of the four different TRPM6 mutations in this small cohort, three had not been previously reported. The long-term prognosis of HSH appears to be good, given early diagnosis and good treatment compliance. This long-term follow-up and prognostic data and the three novel mutations will contribute to the published evidence concerning this rare condition, HSH, and it is hoped will prevent negative outcomes.

Hypomagnesemia is a rare cause of seizures in childhood but should be kept in mind in recurrent and intractable seizures and hypocalcemia in communities where consanguineous marriages are common. Familial hypomagnesemia with secondary hypocalcemia is a rare genetic cause of hypomagnesemia, due to variants in the transient receptor potential melastatin 6 ( TRPM6 ) genes. Here, a three year-old boy with a novel variant in this gene and had difficulties with enteral hypomagnesemia treatment is presented. He had recurrent seizures since two years of age and was diagnosed with epilepsy and treated with multiple antiepileptic drugs. Subsequently, he was diagnosed with rickets due to severe hypocalcemia at another center. The patient was hypotonic and neurodevelopmentally poor. The most prominent laboratory finding was of hypomagnesemia with secondary hypocalcemia. The genetic analysis revealed a novel variant in the TRPM6 gene. After parental treatment of intravenous magnesium (Mg2 + ) sulfate and calcium, the treatment was switched to enteral Mg2 + medications, due to persistent hypomagnesemia and the gastrointestinal side-effects, different oral preparations were used. The patient was stable on an oral maintenance dose of Mg2 + oxide with borderline blood Mg2 + levels and resolution of hypocalcemia. Hypomagnesemia is one of the causes of hypocalcemia. Enteral replacement is the key treatment but the treatment should be individualized for each patient. Normalization of hypomagnesemia is not always easy and should not be the aim of the treatment.

Magnesium (Mg 2+ ) deficiency is probably the most underestimated electrolyte imbalance in Western countries. It is frequent in obese patients, subjects with type-2 diabetes and metabolic syndrome, both in adulthood and in childhood. This narrative review aims to offer insights into the pathophysiological mechanisms linking Mg 2+ deficiency with obesity and the risk of developing metabolic syndrome and type 2 diabetes. Literature highlights critical issues about the treatment of Mg 2+ deficiency, such as the lack of a clear definition of Mg 2+ nutritional status, the use of different Mg 2+ salts and dosage and the different duration of the Mg 2+ supplementation. Despite the lack of agreement, an appropriate dietary pattern, including the right intake of Mg 2+ , improves metabolic syndrome by reducing blood pressure, hyperglycemia, and hypertriglyceridemia. This occurs through the modulation of gene expression and proteomic profile as well as through a positive influence on the composition of the intestinal microbiota and the metabolism of vitamins B1 and D.

The use of vitamin D to reduce the severity of COVID-19 complications is receiving considerable attention, backed by encouraging data. Its purported mode of action is as an immune modulator. Vitamin D, however, also affects the metabolism of phosphate and Mg, which may well play a critical role in SARS-CoV-2 pathogenesis. SARS-CoV-2 may induce a cytokine storm that drains ATP whose regeneration requires phosphate and Mg. These minerals, however, are often deficient in conditions that predispose people to severe COVID-19, including older age (especially males), diabetes, obesity, and usage of diuretics. Symptoms observed in severe COVID-19 also fit well with those seen in classical hypophosphatemia and hypomagnesemia, such as thrombocytopenia, coagulopathy, dysfunction of liver and kidneys, neurologic disturbances, immunodeficiency, failure of heart and lungs, delayed weaning from a respirator, cardiac arrhythmia, seizures, and, finally, multiorgan failure. Deficiencies of phosphate and Mg can be amplified by kidney problems commonly observed in patients with COVID-19 resulting in their wastage into urine. Available data show that phosphate and Mg are deficient in COVID-19, with phosphate showing a remarkable correlation with its severity. In one experiment, patients with COVID-19 were supplemented with a cocktail of vitamin D 3 , Mg, and vitamin B 12 , with very encouraging results. We, thus, argue that patients with COVID-19 should be monitored and treated for phosphate and Mg deficiencies, ideally already in the early phases of infection. Supplementation of phosphate and Mg combined with vitamin D could also be implemented as a preventative strategy in populations at risk.

Magnesium deficiency is to be expected in the population and particularly among risk groups. Magnesium deficiency can cause numerous symptoms, is per se pathological and thus requires treatment. Diagnostics is based on clinical symptoms in conjunction with anamnestic criteria and laboratory parameters. Insufficient magnesium supply is associated with an increased risk for many diseases, e. g. metabolic syndrome, type 2 diabetes and cardiovascular diseases. Magnesium deficiency often appears as comorbidity and may exacerbate diseases. Physicians should pay more attention to magnesium in order to avoid deficits as a cause for multiple symptoms and risk factor for diseases. Optimisation of magnesium status may make an important contribution to the prevention of diseases. Oral magnesium therapy is safe and cost effective., Competing Interests: Oliver Micke: Präsident der Gesellschaft für Magnesium-Forschung e. V.Jürgen Vormann: Vorstand der Gesellschaft für Magnesium-Forschung e. V.Hans-Georg Classen: Vorstand der Gesellschaft für Magnesium-Forschung e. V.Klaus Kisters: Vize-Präsident der Gesellschaft für Magnesium-Forschung e. V., (Thieme. All rights reserved.)

While magnesium deficiency is common and its effects well known on the nervous system, very few studies has been dedicated to the efficiency of magnesium replacement treatments on the central nervous system. In this study, the effects of oral administration of magnesium salts of acetyl-taurinate on the central manifestations of magnesium deficiency is described in rats submitted to low-magnesium diet and in a murine model of Alzheimer's disease. We tested the effect of ATA Mg ® , a salt combining magnesium and taurine, on the hippocampus, a critical component of cognition. 7-10-month-old rats were submitted to dietary magnesium deprivation for 64 days. The effect of magnesium deficiency was studied in ex vivo hippocampal slices. We showed that long-term potentiation of synaptic transmission in the hippocampus was significantly improved by the oral administration of ATA Mg ® at a dose of 50 mg/kg bw/day, which is comparable to the recommended dose in humans. 7-10-months-old transgenic APP/PS1 mice, a model of Alzheimer's disease, received ATA Mg ® during 24 days at a dose of 700 mg/kg bw/day which is the dose used in previous studies demonstrating the positive effect of magnesium supplementation. We showed that long-term potentiation was significantly improved in the treated mice. Moreover, the expression of NR2B subunit of NMDA receptors, known to be involved in synaptic plasticity, was significantly increased in the hippocampus. These results demonstrate the ability of ATA Mg ® to improve the symptoms related to chronic magnesium deficiency at the level of the hippocampus suggesting its bioavailability and effectiveness in reaching the central nervous system.

Proton pump inhibitors are widely prescribed but their long-term use can expose patients to adverse effects. Some of these are not very well known, including hypomagnesemia. Hypomagnesemia can be manifested by cardiac complications such as supraventricular arrhythmia or QT prolongation, increasing the risk of torsade de pointe. We present a case of atrial fibrillation triggered by severe hypomagnesemia secondary to proton pump inhibitor use and exacerbated by thiazide diuretic treatment. Conversion to sinus rhythm showed a prolonged corrected QT interval. We approach the pathophysiology and the electrophysiologic effects of hypomagnesemia., (Copyright © 2020 Elsevier Masson SAS. All rights reserved.)

Magnesium deficiency may occur for several reasons, such as inadequate intake or increased gastrointestinal or renal loss. A large body of literature suggests a relationship between magnesium deficiency and mild and moderate tension-type headaches and migraines. A number of double-blind randomized placebo-controlled trials have shown that magnesium is efficacious in relieving headaches and have led to the recommendation of oral magnesium for headache relief in several national and international guidelines. Among several magnesium salts available to treat magnesium deficiency, magnesium pidolate may have high bioavailability and good penetration at the intracellular level. Here, we discuss the cellular and molecular effects of magnesium deficiency in the brain and the clinical evidence supporting the use of magnesium for the treatment of headaches and migraines.

Migraine is one of the most common recurrent types of headache and is the seventh cause of disability. This neurological disorder is characterized by having pain in head and other various symptoms such as nausea, emesis, photophobia, phonophobia, and sometimes visual sensory disorders. Magnesium (Mg) is a necessary ion for human body and has a crucial role in health and life maintenance. One of the main roles of Mg is to conserve neurons electric potential. Therefore, magnesium deficiency can cause neurological complications. Migraine is usually related to low amounts of Mg in serum and cerebrospinal fluid (CSF). Deficits in magnesium have significant role in the pathogenesis of migraine. Mg has been extensively used in migraine prophylaxis and treatment. This review summarizes the role of Mg in migraine pathogenesis and the potential utilizations of Mg in the prevention and treatment of migraine with the emphasis on transdermal magnesium delivery.

The coordination chemistry of magnesium (Mg 2+ ) was extensively explored. More recently; magnesium; which plays a role in over 80% of metabolic functions and governs over 350 enzymatic processes; is becoming increasingly linked to chronic disease-predominantly due to magnesium deficiency (hypomagnesemia). Supplemental dietary magnesium utilizing biorelevant chelate ligands is a proven method for counteracting hypomagnesemia. However, the coordination chemistry of such bio-relevant magnesium complexes is yet to be extensively explored or elucidated. It is the aim of this review to comprehensively describe what is currently known about common bio-relevant magnesium complexes from the perspective of coordination chemistry.

Background: Preeclampsia is the major cause of maternal morbidity and mortality in developing countries. Magnesium sulfate is considered first-line therapy against eclampsia and magnesium deficiency in pregnancy has been associated with unfavourable perinatal outcomes. However there are doubts if magnesium supplementation during pregnancy can previne preeclampsia especially in population with high nutritional risk. This trial aims to verify the effect of oral magnesium supplmentation on preeclampsia incidence in low income pregnant women., Methods: This randomized, double-blind, placebo-controlled trial investigated the effect of oral magnesium citrate supplementation for preeclampsia in low-income Brazilian pregnant women, i.e. annual per capita income of US$ 1025 or less. Participants were admitted to the study with gestational age between 12 and 20 weeks. Magnesium serum level was measured pre-randomization and participants with hypermagnesemia were excluded. After randomizationg participants received magnesium citrate capsule (300 mg magnesium citrate) or a daily placebo capsule, until delivery. Intent-to-treat analysis was performed., Results: A total of 416 pregnant women were screened and 318 enrolled according to the inclusion criteria; 159 for each arm. Twenty-eight pregnant women were lost to follow-up. 55/290 (18.9%) of pregnant women developed preeclampsia; 26/143 (18.1%) in magnesium group and 29/147 (19.7%) in the control group; OR 0.90 (CI 95% 0.48-1.69), p = 0.747. No cases of eclampsia were registered., Conclusion: Oral magnesium supplementation did not reduce preeclampsia incidence in low-income and low-risk pregnant women., Trial Registration: Registered at ClinicalTrials.gov (Identifier NCT02032186), December 19, 2013.

Background: Bladder-related pain symptoms in patients with bladder pain syndrome/interstitial cystitis (BPS/IC) are often accompanied by depression and memory deficits. Magnesium deficiency contributes to neuroinflammation and is associated with pain, depression, and memory deficits. Neuroinflammation is involved in the mechanical allodynia of cyclophosphamide (CYP)-induced cystitis. Magnesium-L-Threonate (L-TAMS) supplementation can attenuate neuroinflammation. This study aimed to determine whether and how L-TAMS influences mechanical allodynia and accompanying depressive symptoms and memory deficits in CYP-induced cystitis., Methods: Injection of CYP (50 mg/kg, intraperitoneally, every 3 days for 3 doses) was used to establish a rat model of BPS/IC. L-TAMS was administered in drinking water (604 mg·kg -1 ·day -1 ). Mechanical allodynia in the lower abdomen was assessed with von Frey filaments using the up-down method. Forced swim test (FST) and sucrose preference test (SPT) were used to measure depressive-like behaviors. Novel object recognition test (NORT) was used to detect short-term memory function. Concentrations of Mg 2+ in serum and cerebrospinal fluid (CSF) were measured by calmagite chronometry. Western blot and immunofluorescence staining measured the expression of tumor necrosis factor-α/nuclear factor-κB (TNF-α/NF-κB), interleukin-1β (IL-1β), and N-methyl-D-aspartate receptor type 2B subunit (NR2B) of the N-methyl-D-aspartate receptor in the L6-S1 spinal dorsal horn (SDH) and hippocampus., Results: Free Mg 2+ was reduced in the serum and CSF of the CYP-induced cystitis rats on days 8, 12, and 20 after the first CYP injection. Magnesium deficiency in the serum and CSF correlated with the mechanical withdrawal threshold, depressive-like behaviors, and short-term memory deficits (STMD). Oral application of L-TAMS prevented magnesium deficiency and attenuated mechanical allodynia (n = 14) and normalized depressive-like behaviors (n = 10) and STMD (n = 10). The upregulation of TNF-α/NF-κB signaling and IL-1β in the L6-S1 SDH or hippocampus was reversed by L-TAMS. The change in NR2B expression in the SDH and hippocampus in the cystitis model was normalized by L-TAMS., Conclusions: Normalization of magnesium deficiency by L-TAMS attenuated mechanical allodynia, depressive-like behaviors, and STMD in the CYP-induced cystitis model via inhibition of TNF-α/NF-κВ signaling and normalization of NR2B expression. Our study provides evidence that L-TAMS may have therapeutic value for treating pain and comorbid depression or memory deficits in BPS/IC patients.

Introduction: In newborns with the diagnosis of hypoxic-ischemic encephalopathy (HIE) treated with hypother mia, metabolic alterations are observed, which are associated with neurological prognosis. Hypo magnesemia has been reported frequently in the literature in these patients, but it is not measured or corrected in all neonatal healthcare centers., Objective: To evaluate the frequency of hypomag nesemia and hypocalcemia in newborns with HIE treated with whole-body hypothermia and to evaluate the response to the magnesium sulfate administration., Patients and Method: Prospective, observational and descriptive study in hospitalized newborns with the diagnosis of HIE and trea ted with whole-body hypothermia between the years 2016 and 2017. Serial blood measurement of magnesemia (Mg) and calcemia (Ca) was performed. When presenting an Mg level < 1.8 mg/dl, supplementation with magnesium sulfate was administered to maintain levels between 1.9 and 2.8 mg/dl. The frecuency of hypomagnesemia, hypocalcemia and clinical evolution was registered. A descriptive statistical analysis was performed, with central tendency measures., Results: Sixteen ca ses were included, 13 of them presented hypomagnesemia (81.3%), with early-onset (6-36 hours of life), which was normalized with magnesium sulfate treatment, receiving a second dose 4 patients. Six of 16 patients presented hypocalcemia (37.5 %)., Conclusions: Hypomagnesemia is frequent (80%), similar to that described in the literature, and should be controlled and corrected early, given its physiological role, in the same way that calcium is controlled.

The problem of connective tissue dysplasia is currently becoming particularly relevant because of significant increase of individuals with characteristic abnormalities in the structure of connective tissue. The lack of some micronutrients, arising during ontogenesis in the organism, can determine a high risk of worsening connective tissue homeostasis. Recently, the decisive role of magnesium deficiency in the progression of this disease has been demonstrated. The aim of the study was to substantiate the need for magnesium diet therapy in individuals with connective tissue dysplasia basing on the study of the pathogenetic significance of magnesium deficiency in this pathology. Material and methods . The electronic resources of the portals PubMed-NCBI, MEDLINE, the Scientific Electronic Library eLIBRARY.RU, CyberLeninka and the Google Academy were used. Results and discussion . The analysis of the obtained data made it possible to identify fundamentally new provisions on the main mechanisms of the magnesium influence on the metabolic state of all components of connective tissue. It was proved that magnesium deficiency is a predictor of worsening connective tissue homeostasis, increasing in the number of dysplastic symptoms and their severity. This pathogenetically justifies prescribing a balanced diet to patients with connective tissue dysplasia, including products rich in magnesium, taking into account its recommended daily intake, depending on age of patients. Conclusion . Adequate daily intake of magnesium will increase the mechanical properties and functionality of the connective tissue, and should be recommended for patients with connective tissue dysplasia to prevent the development of complications, maintain the quality of life and improve the prognosis for this disease., Competing Interests: The authors declare no overt and potential conflict of interest related to the publication of this article., (Copyright© GEOTAR-Media Publishing Group.)

Background: Pseudohypoparathyroidism(PHP) is a heterogeneous group of disorders due to impaired activation of c AMP dependant pathways following binding of parathyroid hormone (PTH) to its receptor. In PHP end organ resistance to PTH results in hypocalcaemia, hyperphosphataemia and high PTH levels., Case Presentation: A 59 year old male presented with a history of progressive impairment of speech and unsteadiness of gait for 1 week and acute onset altered behavior for 1 day and one episode of generalized seizure. His muscle power was grade four according to MRC (medical research council) scale in all limbs and Chovstek's and Trousseau's signs were positive. Urgent non contrast computed tomography scan of the brain revealed extensive bilateral cerebral and cerebellar calcifications. A markedly low ionized calcium level of 0.5 mmol/l, an elevated phosphate level of 9.5 mg/dl (reference range: 2.7-4.5 mg/dl) and an elevated intact PTH of 76.3 pg/l were noted. His renal functions were normal. His hypocalcemia was accentuated by the presence of hypomagnesaemia. His 25 hydroxy vitamin D level was only marginally low which could not account for severe hypocalcaemia. A diagnosis of pseudohypoparathyroidism without phenotypic defects, was made due to hypocalcaemia and increased parathyroid hormone levels with cerebral calcifications. The patient was treated initially with parenteral calcium which was later converted to oral calcium supplements. His coexisting Vitamin D deficiency was corrected with 1αcholecalciferol escalating doses. His hypomagnesaemia was corrected with magnesium sulphate parenteral infusions initially and later with oral preparations. With treatment there was a significant clinical and biochemical response., Conclusion: Pseudohypoparathyroidism can present for the first time in elderly resulting in extensive cerebral calcifications. Identification and early correction of the deficit will result in both symptomatic and biochemical response.

Background: "Rules of thumb" for the replacement of electrolytes, including magnesium, in critical care settings are used, despite minimal empirical validation of their ability to achieve a target serum concentration. This study's purpose was to evaluate the effectiveness and safety surrounding magnesium replacement in medically, critically ill patients with mild-to-moderate hypomagnesemia., Methods: This was a single-center, retrospective, observational evaluation of episodes of intravenous magnesium replacement ordered for patients with mild-to-moderate hypomagnesemia (1.0-1.9 mEq/L) admitted to a medical intensive care unit from May 2014 to April 2016. The primary effectiveness outcome, achievement of target serum magnesium concentration (≥2 mEq/L) compared to expected achievement using a "rule of thumb" estimation that 1 g intravenous magnesium sulfate raises the magnesium concentration 0.15 mEq/L, was tested using 1-sample z test. Logistic regression analysis was conducted to assess the effect of infusion rate on target achievement., Results: Of 152 days on which magnesium replacements were provided for 72 patients, a follow-up serum magnesium concentration was checked within 24 hours in 89 (58.6%) episodes. Of these 89 episodes, serum magnesium concentration reached target in only 49 (59.8%) episodes compared to an expected 89 (100%; P < .0001). There was no significant association between infusion rate and achievement of the target serum magnesium concentration (odds ratio: 0.962, 95% confidence interval: 0.411-2.256)., Conclusions: Medically, critically ill patients who received nonprotocolized magnesium replacement achieved the target serum magnesium concentration less frequently than the "rule of thumb" estimation predicted.

It is not known whether Teduglutide can allow patients with Short bowel syndrome, previously dependent on continuous or periodic intravenous (IV) magnesium, to attain oral autonomy with or without supplementation. Here, we report on two patients previously dependent on continuous or intermittently administered IV magnesium to achieve autonomy from IV, one with and one without oral supplementation that was previously ineffective in both patients., (Crown Copyright © 2019. Published by Elsevier Inc. All rights reserved.)

Purpose: Hypomagnesemia is a common side effect of panitumumab. The effect of magnesium-containing supplement as a laxative and concomitant antacid (proton pump inhibitor and histamine H 2 antagonist) administration on panitumumab-induced hypomagnesemia was retrospectively investigated., Methods: Patients with advanced or recurrent colorectal cancer who received panitumumab were included in this study. Serum magnesium levels were extracted from the electronic medical records of 1753 administrations in 221 patients who received panitumumab. Serum magnesium levels in patients with or without oral magnesium-containing supplement and antacid treatment were compared using analysis of covariance as the number of panitumumab administration up to 16 times for covariates., Results: The mean serum magnesium levels were significantly decreased with increasing number of panitumumab administrations (2.13 mg/dL at 1st vs. 1.55 mg/dL at 16th, p < 0.001). The use of oral magnesium-containing supplement significantly inhibited the decline in mean serum magnesium level (1.98 mg/dL vs. 1.78 mg/dL, p < 0.001). However, antacid use in patients receiving oral magnesium-containing supplement significantly decreased the effectiveness of the magnesium supplement on serum magnesium level (2.02 mg/dL vs. 1.93 mg/dL, p < 0.05)., Conclusion: The use of oral magnesium-containing supplement might function as magnesium supplement based on the finding that use of oral magnesium-containing supplement during panitumumab administration decreased hypomagnesemia. However, combination of antacid decreased the supplemental effect of oral magnesium on hypomagnesemia. These results suggest the possibility that use of antacids during anti-EGFR antibody administration may promote hypomagnesemia.

Background: Vitamin D and magnesium (Mg) are some of the most studied topics in medicine with enormous implications for human health and disease. Majority of the adults are deficient in both vitamin D and magnesium but continue to go unrecognized by many health care professionals., Areas of Uncertainty: Mg and vitamin D are used by all the organs in the body, and their deficiency states may lead to several chronic medical conditions. Studies described in the literature regarding these disease associations are contradictory, and reversal of any of these conditions may not occur for several years after adequate replacement. One should consider the supplementation therapy to be preventative rather than curative at this time., Data Sources: PubMed search of several reported associations between vitamin D and Mg with diseases., Results: Vitamin D and Mg replacement therapy in elderly patients is known to reduce the nonvertebral fractures, overall mortality, and the incidence of Alzheimer dementia., Conclusions: Vitamin D screening assay is readily available, but the reported lower limit of the normal range is totally inadequate for disease prevention. Based on the epidemiologic studies, ∼75% of all adults worldwide have serum 25(OH)D levels of <30 ng/mL. Because of the recent increase in global awareness, vitamin D supplementation has become a common practice, but Mg deficiency still remains unaddressed. Screening for chronic magnesium deficiency is difficult because a normal serum level may still be associated with moderate to severe deficiency. To date, there is no simple and accurate laboratory test to determine the total body magnesium status in humans. Mg is essential in the metabolism of vitamin D, and taking large doses of vitamin D can induce severe depletion of Mg. Adequate magnesium supplementation should be considered as an important aspect of vitamin D therapy.

The role of magnesium as an analgesic in patients is unclear. Hypomagnesaemia is a common electrolyte abnormality, in the chronic state symptoms are insidious and often non-specific. It is often undiagnosed and thus untreated. There is evidence from animal studies that magnesium is involved in pain control including an animal model of hyperalgesia induced by hypomagnesaemia. We report two cases of patients admitted for pain control which improved when hypomagnesaemia was treated. Each case had metastatic cancer. Both were found on admission to have asymptomatic hypomagnesaemia and were treated with intravenous magnesium. Treatment for hypomagnesaemia resulted in an improvement in pain control such that analgesia was decreased. The incidence of hypomagnesaemia in palliative patients is unknown although it is thought to be common. These cases suggest that treating hypomagnesaemia may improve pain control., Competing Interests: Competing interests: None declared., (© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Hypomagnesaemia can arise from a variety of causes but is particularly prevalent in cancer populations. This case report describes a patient with recurrent symptomatic hypomagnesaemia, on the background of advanced ovarian cancer and a high-output ileostomy, who was successfully managed on a daily continuous subcutaneous infusion of magnesium via a syringe pump. There is limited published information on the subcutaneous administration of magnesium and, to our knowledge, this is the first case to report its routine delivery over 24 hours in a syringe pump. This novel but effective approach for administering magnesium can be delivered in the community and can, therefore, prevent repeated hospital admissions for patients with recurrent symptomatic hypomagnesaemia who would otherwise need intravenous replacement., Competing Interests: Competing interests: None declared., (© Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2018. All rights reserved. No commercial use is permitted unless otherwise expressly granted.)

Vascular calcification (VC) is associated with elevated cardiovascular mortality rates in patients with CKD. Recent clinical studies of patients with advanced CKD have observed an association between low serum magnesium (Mg) levels on one hand and elevated VC and cardiovascular mortality on the other. These findings have stimulated interest in understanding Mg's impact on CKD in general and the associated VC in particular. In vitro and preclinical in vivo data indicate that Mg has the potential to protect vascular smooth muscle cells against calcification via several different molecular mechanisms. Accordingly, data from pilot interventional studies in the clinic suggest that oral Mg supplementation reduces VC in patients with CKD. The present review provides an overview of our current understanding of the impact of Mg on the development of VC in patients with CKD., (Copyright © 2017 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

Magnesium is the most abundant intracellular divalent cation and essential for maintaining normal cellular physiology and metabolism, acting as a cofactor of numerous enzymes, regulating ion channels and energy generation. In the heart, magnesium plays a key role in modulating neuronal excitation, intracardiac conduction, and myocardial contraction by regulating a number of ion transporters, including potassium and calcium channels. Magnesium also has a role in regulating vascular tone, atherogenesis and thrombosis, vascular calcification, and proliferation and migration of endothelial and vascular smooth muscle cells. As such, magnesium potentially has a major influence on the pathogenesis of cardiovascular disease. As the kidney is a major regulator of magnesium homeostasis, kidney disorders can potentially lead to both magnesium depletion and overload, and as such increase the risk of cardiovascular disease. Observational data have shown an association between low serum magnesium concentrations or magnesium intake and increased atherosclerosis, coronary artery disease, arrhythmias, and heart failure. However, major trials of supplementation with magnesium have reported inconsistent benefits and also raised potential adverse effects of magnesium overload. As such, there is currently no firm recommendation for routine magnesium supplementation except when hypomagnesemia has been proven or suspected as a cause for cardiac arrhythmias., (Copyright © 2018 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

Experimental and clinical studies have demonstrated that magnesium deficiency leads to hypertension, insulin resistance, and endothelial dysfunction, and is associated with an increased risk of cardiovascular events. Given that cardiovascular disease and CKD share similar risk factors, the low magnesium status may also contribute to CKD progression. In fact, lower serum magnesium levels and lower dietary magnesium intake are associated with an increased risk of incident CKD and progression to end-stage kidney disease. Because these associations are independent of traditional risk factors, other pathways might be involved in the relationship between magnesium deficiency and the risk of CKD progression. Recent evidence has shown that magnesium suppresses phosphate-induced vascular calcification. Magnesium impairs the crystallization of calcium phosphate-more specifically, the maturation of calciprotein particles. Considering that phosphate overload causes kidney damage, magnesium might counteract the phosphate toxicity to the kidney, as in the case of vascular calcification. This hypothesis is supported by an in vitro observation that magnesium alleviates proximal tubular cell injury induced by high phosphate. Potential usefulness of magnesium as a treatment option for phosphate toxicity in CKD should be further investigated by intervention studies., (Copyright © 2017 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

The objective of the study was to evaluate the efficacy of oral magnesium supplementation in the improvement of metabolic syndrome (MetS) and its components. This is a randomized double-blind, placebo-controlled clinical trial that enrolled 198 individuals with MetS and hypomagnesemia who were randomly allocated to receive either 30 mL of magnesium chloride 5% solution, equivalent to 382 mg of elemental magnesium (n = 100), or placebo solution (n = 98), daily for 16 weeks. Serum magnesium levels <1.8 mg/dL defined hypomagnesemia. At final conditions, a total of 48 (48%) and 76 (77.5%) individuals had MetS in the magnesium and placebo groups (P = 0.01), respectively. At baseline, percent of individuals with 3, 4, and 5 criteria of MetS in the magnesium group were 60.0%, 37.0%, and 3.0%, respectively, and in the control group 55.1%, 35.7%, and 9.2%, respectively. Between basal and final conditions, changes in the components of MetS were significantly higher in the magnesium than placebo groups: -3.6 ± 3.3 mmHg, P = 0.001 for systolic blood pressure; -5.5 ± 1.7 mmHg, P = 0.005 for diastolic blood pressure; -12.4 ± 3.6 mg/dL, P < 0.005 for fasting glucose; -61.2 ± 24 mg/dL, P = 0.003 for triglycerides; and 0.9 ± 0.4 mg/dL, P = 0.06 for high-density lipoprotein cholesterol. Magnesium supplementation improves MetS by reducing blood pressure, hyperglycemia, and hypertriglyceridemia., (Copyright © 2018 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

The bone is the main storage site for Ca 2+ and Mg 2+ ions in the mammalian body. Although investigations into Ca 2+ signaling have progressed rapidly and led to better understanding of bone biology, the Mg 2+ signaling pathway and associated molecules remain to be elucidated. Here, we investigated the role of a potential Mg 2+ signaling-related lysosomal molecule, two-pore channel subtype 2 (TPC2), in osteoclast differentiation and bone remodeling. Previously, we found that under normal Mg 2+ conditions, TPC2 promotes osteoclastogenesis. We observed that under low-Mg 2+ conditions, TPC2 inhibited, rather than promoted, the osteoclast differentiation and that the phosphatidylinositol 3,5-bisphosphate (PI(3,5)P 2 ) signaling pathway played a role in the TPC2 activation under low-Mg 2+ conditions. Furthermore, PI(3,5)P 2 depolarized the membrane potential by increasing the intracellular Na + levels. To investigate how membrane depolarization affects osteoclast differentiation, we generated a light-sensitive cell line and developed a system for the light-stimulated depolarization of the membrane potential. The light-induced depolarization inhibited the osteoclast differentiation. We then tested the effect of myo -inositol supplementation, which increased the PI(3,5)P 2 levels in mice fed a low-Mg 2+ diet. The myo -inositol supplementation rescued the low-Mg 2+ diet-induced trabecular bone loss, which was accompanied by the inhibition of osteoclastogenesis. These results indicate that low-Mg 2+ -induced osteoclastogenesis involves changes in the role of TPC2, which are mediated through the PI(3,5)P 2 pathway. Our findings also suggest that myo -inositol consumption might provide beneficial effects in Mg 2+ deficiency-induced skeletal diseases., (© 2017 by The American Society for Biochemistry and Molecular Biology, Inc.)

Purpose of Review: To update advances in identifying factors affecting magnesium (Mg) status that assist in providing improved evidence-based clinical decision-making for assessing Mg status., Recent Findings: Findings from recent cohort studies, small randomized control trials, and multiple meta-analyses reinforce earlier work that serum Mg concentrations, urinary Mg excretion, and Mg dietary intakes are inversely associated with cardiovascular disease, chronic kidney disease, and diabetes. These studies indicate that the reference range for serum Mg needs updating, and that individuals with serum Mg in the range of 0.75-0.85 mmol/l and displaying changes in other factors associated with a low Mg status may be Mg deficient. Individuals with serum Mg concentrations below this range most likely are Mg deficient and, above this range, are most likely Mg sufficient., Summary: The combined determination of serum Mg concentration, 24-h urinary Mg excretion, and dietary Mg intake is currently the most practical method to obtain a sound assessment of Mg status. The strong correlations of Mg deficiency with increased risk of several chronic diseases, some of which exist as comorbidities, indicate that Mg status should be ascertained in patients presenting such disorder.

Approximately 30% of all cancer patients treated with cisplatin, a widely used broad-spectrum chemotherapeutic agent, experience acute kidney injury (AKI). Almost all patients receiving cisplatin have magnesium (Mg) losses, which are proposed to aggravate AKI. Currently, there are no methods to successfully treat or prevent cisplatin-AKI. Whereas Mg supplementation has been shown to reduce AKI in experimental models and several small clinical trials, the effects of Mg status on tumor outcomes in immunocompetent tumor-bearing mice and humans have not been investigated. The purpose of this study was to further examine the effects of Mg deficiency (±Mg supplementation) on cisplatin-mediated AKI and tumor killing in immunocompetent mice bearing CT26 colon tumors. Using a model where cisplatin alone (20 mg/kg cumulative dose) produced minimal kidney injury, Mg deficiency significantly worsened cisplatin-mediated AKI, as determined by biochemical markers (blood urea nitrogen and plasma creatinine) and histological renal changes, as well as markers of renal oxidative stress, inflammation, and apoptosis. By contrast, Mg supplementation blocked cisplatin-induced kidney injury. Using LLC-PK 1 renal epithelial cells, we observed that Mg deficiency or inhibition of Mg uptake significantly enhanced cisplatin-induced cytotoxicity, whereas Mg supplementation protected against cytotoxicity. However, neither Mg deficiency nor inhibition of Mg uptake impaired cisplatin-mediated killing of CT26 tumor cells in vitro. Mg deficiency was associated with significantly larger CT26 tumors in BALB/c mice when compared with normal-fed control mice, and Mg deficiency significantly reduced cisplatin-mediated tumor killing in vivo. Finally, Mg supplementation did not compromise cisplatin's anti-tumor efficacy in vivo., (Copyright © 2017 the American Physiological Society.)

Background Hypomagnesaemia is a relatively-common side effect of some systemic anti-cancer therapies (SACT). Oral and intravenous magnesium (given as injections or short infusions) have problems arising from their poor tolerability, and need for frequent administrations, respectively. Objective Assessing the effectiveness and safety of weekly continuous magnesium infusions (CMI) in the management of SACT-related hypomagnesaemia. Methods CMIs (initiated at 10 mmol/day and up-titrated subject to response) were prescribed to patients with ≥3 magnesium readings <0.5 mmol/L despite intravenous replacement with bolus-or-short-infusions (BSI). Efficacy (compared to BSI): (a) reduction in the number of moderate/severe hypomagnesaemia episodes, and (b) increase in mean magnesium serum levels., Safety: non-occurrence of grade ≥3 toxicities (according to the common terminology criteria for adverse events v4). Results Three patients were treated (mean age: 62-years), pre-SACT levels were 0.629 ± 0.121 mmol/L., Efficacy: (a) 1 versus 18 episodes; (b) 0.639 ± 0.093 mmol/L versus 0.533 ± 0.191 mmol/L. All comparisons were statistically significant in favour of CMI (p < 0.001). No magnesium-related grade ≥2 side effects were observed. Conclusion CMIs resulted in a marked reduction in the number of episodes of hypomagnesaemia and higher magnesium levels, with no significant side effects. CMIs represent a potential option for the management of SACT-related hypomagnesaemia, although further research in an expanded cohort is required.

In the following review, we evaluated the current literature and evidence-based data on transdermal magnesium application and show that the propagation of transdermal magnesium is scientifically unsupported. The importance of magnesium and the positive effects of magnesium supplementation are extensively documented in magnesium deficiency, e.g., cardiovascular disease and diabetes mellitus. The effectiveness of oral magnesium supplementation for the treatment of magnesium deficiency has been studied in detail. However, the proven and well-documented oral magnesium supplementation has become questioned in the recent years through intensive marketing for its transdermal application (e.g., magnesium-containing sprays, magnesium flakes, and magnesium salt baths). In both, specialist and lay press as well as on the internet, there are increasing numbers of articles claiming the effectiveness and superiority of transdermal magnesium over an oral application. It is claimed that the transdermal absorption of magnesium in comparison to oral application is more effective due to better absorption and fewer side effects as it bypasses the gastrointestinal tract., Competing Interests: The authors declare no potential conflict of interest.

Magnesium is essential to the proper functioning of numerous cellular processes. Magnesium ion (Mg 2+ ) deficits, as reflected in hypomagnesemia, can cause neuromuscular irritability, seizures and cardiac arrhythmias. With normal Mg 2+ intake, homeostasis is maintained primarily through the regulated reabsorption of Mg 2+ by the thick ascending limb of Henle's loop and distal convoluted tubule of the kidney. Inadequate reabsorption results in renal Mg 2+ wasting, as evidenced by an inappropriately high fractional Mg 2+ excretion. Familial renal Mg 2+ wasting is suggestive of a genetic cause, and subsequent studies in these hypomagnesemic families have revealed over a dozen genes directly or indirectly involved in Mg 2+ transport. Those can be classified into four groups: hypercalciuric hypomagnesemias (encompassing mutations in CLDN16, CLDN19, CASR, CLCNKB), Gitelman-like hypomagnesemias (CLCNKB, SLC12A3, BSND, KCNJ10, FYXD2, HNF1B, PCBD1), mitochondrial hypomagnesemias (SARS2, MT-TI, Kearns-Sayre syndrome) and other hypomagnesemias (TRPM6, CNMM2, EGF, EGFR, KCNA1, FAM111A). Although identification of these genes has not yet changed treatment, which remains Mg 2+ supplementation, it has contributed enormously to our understanding of Mg 2+ transport and renal function. In this review, we discuss general mechanisms and symptoms of genetic causes of hypomagnesemia as well as the specific molecular mechanisms and clinical phenotypes associated with each syndrome.

Dietary supplementation with magnesium (Mg) in addition to classical therapies for diabetes may help in prevention or delaying of diabetic complications.We aimed to evaluate the status of serum Mg in children with type 1 diabetes and assessing its relationship to glycemic control and lipid profile. Then evaluating the effect of oral Mg supplementation on glycemic control and lipid parameters.We included 71 children at Pediatric Endocrinology Outpatient Clinic, Zagazig University, Egypt with type 1 diabetes and assessed HBA1c, lipid profile, and serum Mg at the start of study. Patients with serum Mg level < 1.7 mg/dL were given 300 mg Mg oxide for 3 months. After that we reevaluated HBA1c, lipid profile, and serum Mg in all patients.The study included 71 patients with type 1 diabetes (32 males and 39 females); their mean age was 9.68 ± 3.99 years. The mean serum Mg level was 1.83 ± .27 mg/dL. Hypomagnesemia was detected in 28.2% study patients. Serum Mg was found to be positively correlated with high density lipoprotein, mean corpuscular volume and platelet count (P < 0.001), and negatively correlated with age, HbA1c, triglycerides, total cholesterol, low density lipoprotein, and duration of diabetes (P < 0.001). There was significant reduction in HBA1c in group given Mg supplementation. HBA1c was initially 10.11% ± 0.87%. After 3 months of oral Mg supplementation it is reduced to 7.88% ± 0.42% (P < 0.001). There was statistically significant difference in lipid parameters in hypomagnesemic diabetic patients before and after Mg supplementation with significant reduction in serum triglycerides, LDL, and total cholesterol following Mg supplementation with P < 0.001. Although HDL shows a significant increase after Mg supplementation in hypomagnesemic diabetic children with P < 0.001.Correction of hypomagnesemia in type 1 diabetic children with oral Mg supplements is associated with optimization of glycemic control and reduction of atherogenic lipid fraction as well as increase in protective lipid fraction.

Objectives: The aim of this study was to determine the effect of magnesium supplementation on the depression status of depressed patients suffering from magnesium deficiency., Methods: Sixty depressed people suffering from hypomagnesemia participated in this trial. The individuals were randomly categorized into two groups of 30 members; one receiving two 250-mg tablets of magnesium oxide (MG) daily and the other receiving placebo (PG) for 8 wk. The Beck Depression Inventory-II was conducted and the concentration of serum magnesium was measured., Results: At the end of intervention, 88.5% of the MG and 48.1% of the PG (P = 0.002) had a normal level of magnesium. The mean changes of serum magnesium were significantly different across the two groups. After the intervention, the mean Beck score significantly declined. However, in the MG, this reduction was more significant than in the PG (P = 0.02), so that the mean changes in this group experienced 15.65 ± 8.9 reduction, but in the PG, it declined by 10.40 ± 7.9., Conclusions: Daily consumption of 500 mg magnesium oxide tablets for ≥8 wk by depressed patients suffering from magnesium deficiency leads to improvements in depression status and magnesium levels. Therefore, assessment of the magnesium serum and resolving this deficiency positively influence the treatment of depressed patients., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Purpose: Magnesium supplementation is an effective protective method against cisplatin-induced nephrotoxicity (CIN); however, there are few reports regarding the mechanism of its nephroprotective effect. The aim of this study was to determine whether premedication with intravenous magnesium prevents CIN and to determine the relationship between its nephroprotective effect and serum magnesium level., Methods: Fifty-eight patients with head and neck cancer who received cisplatin, docetaxel, and 5-fluorouracil (DCF) were retrospectively investigated. Grade 2 or more serum creatinine elevation was defined as CIN. The incidence of CIN was compared between a magnesium sulfate (20 mEq, 2.46 g) premedication group and a non-magnesium group during the first cycle and in all cycles., Results: CIN did not occur in any patients receiving magnesium premedication but did occur in 5 of 29 patients during the first cycle and in 6 patients during all subsequent cycles in patients who did not receive magnesium premedication. Furthermore, the variation of creatinine clearance was significantly worse in the non-magnesium group than in the magnesium premedication group from baseline. There was no difference in adverse effects or response rate between the two groups. Univariate analysis suggested that magnesium premedication significantly reduced the risk of CIN. On the other hand, serum magnesium depletion was seen in both groups to equal degrees despite supplementation., Conclusion: Intravenous magnesium premedication has a protective effect on cisplatin-induced nephrotoxicity without the influence on the serum magnesium level. Magnesium premedication is a simple nephroprotective method that does not influence other adverse effects or rate of response to chemotherapy.