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BACKGROUND: Chronic hypomagnesemia is commonly due to diarrhea, alcoholism, and drugs. More rarely, it is caused by genetic defects in the effectors of renal magnesium reabsorption. METHODS: In an adult patient with acquired severe hypomagnesemia, hypocalcemia, tubulointerstitial nephropathy, and rapidly progressing kidney injury, similarities between the patient’s presentation and features of genetic disorders of renal magnesium transport prompted us to investigate whether the patient had an acquired autoimmune cause of renal magnesium wasting. To determine if the patient’s condition might be explained by autoantibodies directed against claudin-16 or claudin-19, transmembrane paracellular proteins involved in renal magnesium absorption, we conducted experiments with claudin knockout mice and transfected mouse kidney cells expressing human claudin-16 or claudin-19. We also examined effects on renal magnesium handling in rats given intravenous injections of IgG purified from sera from the patient or controls. RESULTS: Experiments with the knockout mice and in vitro transfected cells demonstrated that hypomagnesemia in the patient was causally linked to autoantibodies directed against claudin-16, which controls paracellular magnesium reabsorption in the thick ascending limb of Henle’s loop. Intravenous injection of IgG purified from the patient’s serum induced a marked urinary waste of magnesium in rats. Immunosuppressive treatment combining plasma exchange and rituximab was associated with improvement in the patient’s GFR, but hypomagnesemia persisted. The patient was subsequently diagnosed with a renal carcinoma that expressed a high level of claudin-16 mRNA. CONCLUSIONS: Pathogenic claudin-16 autoantibodies represent a novel autoimmune cause of specific renal tubular transport disturbances and tubulointerstitial nephropathy. Screening for autoantibodies targeting claudin-16, and potentially other magnesium transporters or channels in the kidney, may be warranted in patients with acquired unexplained hypomagnesemia.

Magnesium is the fourth most abundant cation in the human body, essential for physiological processes and is the electrolyte with levels commonly deranged in critically ill patients. These derangements of magnesium imbalance can go unnoticed and result in poor clinical outcomes, requiring both worthy attention to abnormal values and accurate tools and methods to measure magnesium reliably. At present, clinical laboratories employ various methodologies for measuring magnesium in blood and urine. This review aims to address the role of magnesium from not only physiological and pathophysiological perspectives, but importantly to review the methods for measuring magnesium with relevant analytical considerations. Given the role of magnesium and drugs for various treatments, measuring magnesium has become more relevant as drugs can lead to magnesium imbalances. Clinical manifestations and etiology of magnesium imbalance as divided into hypomagnesemia and hypermagnesemia are also reviewed.

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.

Studies on the association between serum magnesium level and prediabetes yielded inconsistent results. Therefore, the present meta-analysis was designed to examine the association between serum magnesium levels and prediabetes. Online databases including PubMed, Embase, Scopus and Google Scholar were searched up to October, 2020. A total of 10 studies that reported mean and standard deviation (SD) of magnesium levels in prediabetes and healthy control group were identified. Random effects models were used to pool weighted mean differences (WMDs) of serum magnesium levels. Pooled-analysis showed that subjects with prediabetes had significantly lower serum magnesium levels compared with healthy controls (WMD = − 0.07 mmol/L; 95% CI − 0.09, − 0.05 mmol/L, P 2 = 95.6%, P

Background. Primary hypomagnesemia with secondary hypocalcemia (HSH) is a rare genetic disorder. Dysfunctional transient receptor potential melastatin 6 causes impaired intestinal absorption of magnesium, leading to low serum levels accompanied by hypocalcemia. Typical signs at initial manifestation are generalized seizures, tetany, and/or muscle spasms. Case report. We present a 5 w/o female manifesting tonic-clonic seizures. Laboratory tests detected severe hypomagnesemia and hypocalcemia. The molecular genetic analysis revealed two novel mutations within the TRPM6 gene c.3308dupC (p.Pro1104Thrfs*28) (p.P1104Tfs*28) and c.3958C>T (p.Gln1302*) (p.Q1302*) and the patient was successfully treated with Mg supplementation. Conclusion. Ion disbalance should be taken into account in the differential diagnosis of infantile seizures. Accurate diagnosis of HSH together with appropriate treatment are crucial to prevent irreversible neurological outcomes.

The present study aimed to investigate the incidence of preoperative ionized hypomagnesemia and compare with that of total hypomagnesemia.This prospective observational study included 536 patients aged20 years who were scheduled for elective surgery. Total and ionized magnesium levels were evaluated before and after the surgery. Based on these levels, patients were classified into the following groups: ionized hypo- (0.42 mmol/L), normo- (0.42-0.59 mmol/L) and hypermagnesemia (0.59 mmol/L), as well as total hypo- (1.9 mg/dL[0.78 mmol/L]), normo- (1.9-2.7 mg/dL[0.78-1.11 mmol/L]) and hypermagnesemia (2.7 mg/dL [1.11 mmol/L]). The primary objective was to establish the incidence of preoperative ionized hypomagnesemia.There was a marked difference between the incidence of preoperative ionized and total hypomagnesemia (28% vs. 19%; p0.001). The postoperative values of ionized magnesium, ionized calcium, and albumin were significantly lower than the respective preoperative values (p0.001 for all three variables).The incidence of hypomagnesemia, determined by ionized magnesium concentration, was higher than that determined by total magnesium concentration.

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.

Vascular endothelial cells have a critical role in the maintenance of cardiovascular function. Evidence suggests that endothelial function may be compromised under conditions of magnesium deficiency, which increases vulnerability to inflammation. Whole genome transcription analysis was used to explore the acute (24 h) effects of magnesium on human umbilical vascular endothelial cells (HUVEC) cultured in low (0.1 mM) or high (5 mM) concentrations. With low magnesium 2728 transcripts were differentially expressed compared to the 1 mM control cultures and 3030 were differentially expressed with high magnesium. 615 transcripts were differentially expressed under both conditions, of which only 34 showed a concentration-dependent response. Analysis indicated that cellular organisation and biogenesis and key cellular processes such as apoptosis were impacted by both low and high conditions. High magnesium also influenced protein binding functions, intracellular signal transduction, metabolic and catalytic processes. Both conditions impacted on stress-related processes, in particular the inflammatory response. Key mediators of calcium-dependent regulation of gene expression were responsive to both high and low magnesium conditions. The HUVEC transcriptome is highly sensitive to acute changes in the concentration of magnesium in culture medium. The findings of this study support the view that whilst inflammation is an important process that is responsive to magnesium, the function of the endothelium may be impacted by other magnesium-induced changes including maintenance of cellular integrity, receptor expression and metabolic functions. The high proportion of transcripts that did not show a concentration-dependent response suggests variation in magnesium may elicit indirect changes, possibly mediated by other ions.

Magnesium (Mg) is critically involved in the pathophysiology of multiple human diseases; nevertheless, Mg disorders are often poorly considered in the clinical practice. To update the prevalence and incidence of hypomagnesemia and hypermagnesemia in a real-life scenario, which better represents clinical practice, we analyzed data from 12,696 patients whose Mg serum levels were measured from January 1, 2015, through December 31, 2017 at our University Hospital. Hypomagnesemia and hypermagnesemia were defined by Mg concentrations 3.8 mg/dL (1.5 mmol/L), in accordance with the reference values for magnesemia of our laboratory (1.5-3.8 mg/dL). The prevalence of hypomagnesemia and hypermagnesemia was 8.43% (n=1071) and 1.78% (n=226), respectively. Hypomagnesemia occurred more frequently in females compared with males [53.3% (n=560) versus 47.7% (n=511), χ2=4.03, p

Adequate magnesium intakes are associated with lower diabetes, hypertension, and cardiovascular disease (CVD) risk but are low in modern diets. Magnesium DRIs, estimated using standard reference body weights (SRBWs) lower than current mean US adult body weights (BWs), need revision. Magnesium DRIs assume variance at 10% CV, whereas balance study data suggests 20–30% CV. Here, estimated average requirements (EARs), the DRI measure estimating average magnesium requirements for healthy adults, were corrected using 2011–2014 mean US adult BWs. Magnesium EARs (in mg magnesium/d) increased 17% for men (330–350 to 386–409) and 25% for women (255–265 to 319–332). RDAs, the DRI measure meant to cover the magnesium needs of 98% of healthy adults, were calculated using BW-corrected EARs given 3 CV levels: 1) 10% (assumed in 1997 DRIs), 2) 20% (model-derived variance from USDA magnesium studies), and 3) 30% (using USDA plus older human magnesium balance data). BW-corrected magnesium RDAs (in mg magnesium/d) rose from 400–420 and 310–320 for men and women, respectively, to 1) 463–491 and 383–398 (16.5% and 23.5% increases), 2) 540–573 and 447–465 (35.5% and 44.5% increases), and 3) 617–654 and 511–531 (55% and 65.5% increases). These recalculations move magnesium intakes estimated to prevent disease into ranges found in traditional diets and to intake levels shown to lower hypertension, diabetes, and CVD risk. In conclusion, mean BW rises over the last ≥20 y and data-driven estimates of CV indicate that reliable US adult magnesium RDAs are ≥60–235 and 70–210 mg magnesium/d higher for men and women, respectively, than the current 1997 RDAs. US adult BMIs are 25 with actual mean BWs. Adjustments for rising BW are necessary for magnesium DRIs to remain useful tools for defining magnesium intake adequacy/deficiency.

Magnesium, known as "the forgotten electrolyte", is an essential element of life. Magnesium deficiency is implicated in many diseases, including liver cirrhosis. This study aimed to explore the prevalence of magnesium deficiency in liver cirrhosis and investigate the relationship between magnesium levels and complication of liver cirrhosis and clinical outcomes.Cirrhotic patients with serum magnesium levels measured were retrospectively identified from 2016 to 2017. Demographics, laboratory parameters, complications were collected. The Child-Pugh class, MELD score, and ALBI score were calculated.The mean serum magnesium level of all 152 patients was lower than the normal, including 92 patients diagnosed with magnesium deficiency. Compared to Child-Pugh class A, magnesium levels were significantly lower in the patients with Child-Pugh class B or C (Magnesium deficiency is highly prevalent in cirrhotic patients. Magnesium deficiency is related to worse transplant-free survival, infection and the severity of liver cirrhosis.

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.

Purpose: To evaluate the effects of low blood magnesium levels on the optic nerve, retina, and retinal vascular structure.Methods: This observational and cross-sectional study was conducted between...

Background and aims Magnesium is a fundamental cation that regulates neuronal transmission, protein synthesis, energy metabolism. Magnesium deficiency mostly affects nervous and cardiovascular systems determining weakness, tremors, seizure and arrhythmias. This condition retains also a role in memory function and neuronal plasticity. Importantly magnesium deficiency could remain latent and asymptomatic resulting a risk factor for cardiovascular disease. In this sense we aim to determine magnesium status in patient presenting cognitive impairment of vascular origin. Methods 21 healthy subjects and 27 patients presenting vascular cognitive impairment were included in this study. Both plasma and intraerythrocitary magnesium level were measured to detect magnesium deficiency and cognitive performance was evaluated trough Mini Mental State Evaluation (MMSE). Results Here we showed that patients presenting vascular cognitive impairment present intraerythrocitary magnesium level lower than age-matched healthy subjects. To note their plasma magnesium resulted within reference limit. Conclusion We suggest that intracellular magnesium laboratory measurement is needed to detect occult magnesium deficiency in population at risk. Magnesium supplementation could represent an adjuvant for healthy aging in high risk population.

Diabetes mellitus is a group of common metabolic disorders that share the phenotype of hyperglycaemia. Like most other chronic disorders, diabetes increases the excretion of minerals and other nutrients. Magnesium is a micronutrient and the second most abundant intracellular cation whose concentration remains remarkably constant in healthy subjects. It is known to activate enzymes and act as important cofactor in various biochemical reactions. Also, Magnesium is required for insulin secretion and for proper insulin functioning via tyrosine kinase activity at the receptor level. Therefore, through this study an attempt has been made to evaluate the association between serum magnesium levels and the glycaemic status of these patients as measured in the form of HbA1c.The study is conducted in the General Medicine ward of a tertiary care hospital in Assam for 4 months, which included 140 patients of Type 2 Diabetes Mellitus. Patients were subjected to history and examination, investigations and analysed using simple statistical methods.In the present study, HbA1C ofgt;7% was taken as poor glycaemic control and the mean magnesium level in this group was 1.46±0.50 mg/dl and in the group withlt;7% indicated good glycaemic control, the mean magnesium level was 1.48±0.53 mg/dl. On doing t-test for independent means, the p-value was found to be significant atlt;0.00001. This shows that patients with poor glycaemic control(HbA1cgt;7%) have lesser serum magnesium levels as compared to the patients with good glycaemic control(HbA1clt;7%).The present study investigated the serum magnesium levels in patients with Type 2 Diabetes Mellitus and its association with glycated haemoglobin (HbA1c) levels. It was found that the level of magnesium was lower in patients with higher glycated hemoglobin levels. Therefore hypomagnesemia was more in patients with poor glycaemic control. Based on this study, it can be said that magnesium levels can be taken as an indicator of the glycaemic status in the diabetics. Oral magnesium supplementation can be advised in such patients.

Multi-system effects of diabetes mellitus such as retinopathy, nephropathy, neuropathy and cardiovascular diseases are important public health concerns. A number of studies have reported the association between magnesium (Mg) and diabetes and its complications. However, conclusions were inconsistent. The Objective is to estimate level of serum magnesium in the development and progression of DM Type 2 and its complications.The present study was conducted in the Department of Medicine, S.P. Medical Collegeamp; Associated Group of Hospitals, Bikaner over a period of 6 months. The study design was a cross sectional study.In this study 50.4% of the patients were males and 49.6% were females. Overall, mean age of the study population was 48± 18 years. The mean BMI of the study population was 26.43 + 5.11 kg/m2.In this study majority of the patients with hypomagnesemia Mglt; 1.7mg/ dl were having diabetic complication, mainly microvascular complications. Patient with hypomagnesemia were showing significant association with nephropathy (plt;0.001, r= -0.48), neuropathy (plt;0.009), retinopathy (plt;0.007) and cardiovascular disease (plt; 0.001).The study did not show significant correlation with hypertension and cerebrovascular events.Measurement of serum magnesium should be considered in patients whose blood sugar is uncontrolled with anti diabetic drugs or insulin, as hypomagnesemia may be a cause for micro vascular complications of diabetes. Supplementation of magnesium is also cost effective and should be done if patient is found hypomagnesemia.Magnesium levels correlate with Microvascular complications specially Nephropathy.

Producción Científica, Magnesium (Mg) is an essential micronutrient that participates in various enzymatic reactions that regulate vital biological functions. The main aim was to assess the Mg status and its association with nutritional indicators in seventeen cystic fibrosis (CF) patients. The serum Mg and calcium (Ca) levels were determined using standardized methods and the dietary Mg intake by prospective 72 h dietary surveys. The mean serum Ca (2.45 mmol/L) and Mg (0.82 mmol/L) had normal levels, and the mean dietary intake of the Ca (127% DRI: Dietary Reference Intake) and Mg (125% DRI) were high. No patients had an abnormal serum Ca. A total of 47% of the subjects had hypomagnesemia and 12% insufficient Mg consumption. One patient had a serum Mg deficiency and inadequate Mg intake. A total of 47 and 82% of our series had a high serum Ca/Mg ratio of >4.70 (mean 4.89) and a low Ca/Mg intake ratio of

Background Low Magnesium (Mg) dietary intake has been associated with increased risk of type 2 diabetes mellitus (T2DM). Furthermore, in patients with T2DM, hypomagnesemia is associated with worst glycaemic control. Bariatric surgery (BS) remains the most effective treatment in severe obesity and also provides resolution/improvement of T2DM. Our aim is to evaluate the association between Mg supplementation post-BS and Mg serum levels with diabetes status after BS. Methods We performed an observational study on patients with obesity and T2DM who underwent BS. Data was assessed pre-BS and one-year post-BS. Results We included a total of 403 patients with T2DM. At baseline, 43.4% of the patients had Mg deficiency. Pre-BS, patients with Mg deficiency had poorer glycaemic control – HbA1c 7.2 ± 1.6% vs 6.4 ± 1.0% (p vs 117.5 ± 36.6 mg/dL (p vs 1.0 (IQR 0–1.0) (p = 0.002). These findings persisted at one-year post-BS. At the first-year post-BS, 58.4% of the patients had total remission of T2DM and 4.1% had partial remission. Patients without Mg deficiency at one-year post-BS had higher rates of total and partial remission. Higher serum Mg levels at baseline is an independent predictor of total T2DM remission (p Conclusion In patients with T2DM submitted to BS, higher Mg serum levels at baseline and 1-year after BS were associated with better glycaemic control and higher rates of total T2DM remission at the first year post-BS.

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 D3, Mg, and vitamin B12, 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.In der Bevölkerung und vor allem bei Risikogruppen muss mit Magnesiummangel gerechnet werden. Magnesiummangel kann zahlreiche Symptome verursachen, ist per se pathologisch und deshalb therapiebedürftig. Die Diagnostik stützt sich auf die klinische Symptomatik in Verbindung mit anamnestischen Hinweisen und Laborparametern. Eine schlechte Magnesiumversorgung ist mit einem erhöhten Risiko für zahlreiche Erkrankungen assoziiert, darunter metabolisches Syndrom, Diabetes mellitus Typ 2 und Herz-Kreislauf-Erkrankungen. Magnesiummangel tritt häufig auch als Komorbidität auf und kann zur Exazerbation von Krankheiten beitragen. Magnesium sollte eine größere Aufmerksamkeit geschenkt werden, um Mangelzustände als Ursache vielfältiger Symptome sowie als Risikofaktor für Erkrankungen zu vermeiden. Eine Optimierung der Magnesiumversorgung kann einen wichtigen Beitrag in der Prävention leisten. Die orale Magnesiumtherapie ist unbedenklich und kostengünstig.

BACKGROUND: Prior research has confirmed that persistent hypomagnesemia was predictive of shorter survival among patients with ovarian cancer who received carboplatin-based chemotherapy. In the current retrospective study, the authors examined the association between hypomagnesemia and survival in patients with head and neck cancer who received concurrent chemoradiation with weekly infusions of cisplatin and/or carboplatin. METHODS: Patients with head and neck cancers who had undergone chemoradiation with cisplatin and/or carboplatin between January 1, 2010, and December 31, 2014, were included. Patients were aged ≥18 years with pathology of squamous cell carcinoma of the larynx, oral cavity, or oropharynx who had received at least 30 fractions of radiotherapy with concurrent weekly cisplatin and/or carboplatin. Pathology features, laboratory results, Eastern Cooperative Oncology Group performance status, social histories, and survival were recorded. The association between hypomagnesemia and survival was analyzed controlling for known prognostic factors. RESULTS: The final cohort consisted of 439 patients with a median age of 59 years. A greater frequency of hypomagnesemia during the treatment course was found to be significantly associated with shorter survival (hazard ratio [HR], 1.13; P = .033) independent of age (HR, 1.65; P = .042), cancer site (nonoropharynx vs oropharynx: HR, 2.15 [P = .003]), Eastern Cooperative Oncology Group performance status (>1 vs ≤1: HR, 2.64 [P < .001]), and smoking history (smoker vs nonsmoker: HR, 1.88 [P = .012]). In addition, more severe hypomagnesemia was associated with shorter survival compared with the milder form. CONCLUSIONS: The frequency and severity of hypomagnesemia during treatment are prognostic of survival for patients with head and neck cancers who are receiving concurrent chemoradiation with cisplatin and/or carboplatin. A prospective study is needed to investigate the impact of the prevention of hypomagnesemia on survival in this patient population.

Magnesium (Mg) is the second most frequent intracellular cation in humans with a critical role in insulin metabolism and glucoregulation. Women with polycystic ovary syndrome (PCOS) often present with insulin resistance and impaired glucoregulatory status; however, their Mg status remains unclear. Therefore, we aimed to conduct a systematic review and meta-analysis to evaluate serum Mg concentration in women with PCOS and compare it with that of controls without PCOS. Online databases of PubMed, Scopus, Cochrane Library, and ISI Web of Science were searched for studies evaluating the relationship between Mg concentrations and PCOS status until October 2019. Pooled weighted mean differences (WMDs) of serum Mg levels were calculated using random effects models. A total of eight studies (10 arms; n = 2026 women) were included. Pooled effect sizes, expressed as WMD and 95% CI, revealed decreased serum Mg concentrations in women with PCOS compared with controls (− 0.09 (− 0.17, − 0.02) mmol/L; P = 0.01). However, significant heterogeneity was detected across the studies (I 2 = 98.0%, P

Magnesium (Mg) plays important roles in maintaining genomic stability and cellular redox. Mg also serves as nature's physiological calcium (Ca) channel antagonist, controlling intracellular Ca entry. Because Ca is the most important second messenger, its intracellular concentration is tightly regulated. Excess intracellular Ca can activate aberrant signaling pathways leading to the acquisition of pathological characteristics and cell injury. Several epidemiological studies have linked Mg deficiency (MgD) and increased Ca:Mg ratios with higher incidences of colon cancer and increased mortality. While it is estimated that less than 50% of the US population consumes the recommended daily allowance for Mg, Ca supplementation is widespread. Therefore, we studied the effect of MgD, with variable Ca:Mg ratios on cellular oxidative stress, cell migration, calpain activity, and associated signaling pathways using the CT26 colon cancer cell line. MgD (with Ca:Mg ratios >1) elevated intracellular Ca levels, calpain activity and TRPM7 expression, as well as oxidative stress and cell migration, consistent with observed degradation of full-length E-cadherin, β-catenin, and N-terminal FAK. MgD was accompanied by enhanced degradation of IκBα and the transactivation domain containing the C-terminus of NF-κB p65 (RelA). MgD-exposed CT26 cells exhibited increased p53 degradation and aneuploidy, markers of genomic instability. By contrast, these pathological changes were not observed when CT26 were cultured under MgD conditions where the Ca:Mg ratio was kept at 1. Together, these data support that exposure of colon cancer cells to MgD with physiological Ca concentrations (or increasing Ca:Mg ratios) leads to the acquisition of a more aggressive, metastatic phenotype.

"X-linked immunodeficiency with magnesium defect, Epstein-Barr virus (EBV) infection, and neoplasia" (XMEN) disease is an inborn error of glycosylation and immunity caused by loss of function mutations in the magnesium transporter 1 (MAGT1) gene. It is a multisystem disease that strongly affects certain immune cells. MAGT1 is now confirmed as a non-catalytic subunit of the oligosaccharyltransferase complex and facilitates Asparagine (N)-linked glycosylation of specific substrates, making XMEN a congenital disorder of glycosylation manifesting as a combined immune deficiency. The clinical disease has variable expressivity, and impaired glycosylation of key MAGT1-dependent glycoproteins in addition to Mg2+ abnormalities can explain some of the immune manifestations. NKG2D, an activating receptor critical for cytotoxic function against EBV, is poorly glycosylated and invariably decreased on CD8+ T cells and natural killer (NK) cells from XMEN patients. It is the best biomarker of the disease. The characterization of EBV-naive XMEN patients has clarified features of the genetic disease that were previously attributed to EBV infection. Extra-immune manifestations, including hepatic and neurological abnormalities, have recently been reported. EBV-associated lymphomas remain the main cause of severe morbidity. Unfortunately, treatment options to address the underlying mechanism of disease remain limited and Mg2+ supplementation has not proven successful. Here, we review the expanding clinical phenotype and recent advances in glycobiology that have increased our understanding of XMEN disease. We also propose updating XMEN to "X-linked MAGT1 deficiency with increased susceptibility to EBV-infection and N-linked glycosylation defect" in light of these novel findings.

Magnesium (Mg2+) is the second most abundant intracellular and fourth extracellular cation found in the body and is involved in a wide range of functions in the human cell and human physiology. Its role in most of the enzyme processes (ATP-ases)-stabilisation of nucleic acids (DNA, RNA), regulation of calcium and potassium ion channels, proliferation, glucose metabolism and apoptosis-make it one of the most important cations in the cell. Three pathogenetic mechanisms are mainly implicated in the development of hypomagnesaemia: reduced food intake, decreased intestinal absorption and increased renal excretion of Mg2+. This review presents the function of Mg2+, how it is handled in the kidney and the drugs that cause hypomagnesaemia. The frequency and the number of drugs like diuretics and proton-pump inhibitors (PPIs) that are used daily in medical practice are discussed in order to prevent and treat adverse effects by providing an insight into Mg2+ homeostasis.

International audience; More and more studies are accumulating about COVID-19. Some aspects of the pathogenesis of the disease recall events occurring in Mg deficiency, such as a drop of T cells, increased plasma concentration of inflammatory cytokines, and endothelial dysfunction. We hypothesize that a low Mg status, which is rather common, might foment the transition from mild to critical clinical manifestations of the disease. Epidemiological, clinical, and fundamental research is needed to clarify the potential role of Mg deficiency in COVID-19.

Epidemiological studies on magnesium intake and primary liver cancer (PLC) are scarce, and no prospective studies have examined the associations of magnesium intake with PLC incidence and mortality. We sought to clarify whether higher magnesium intake from diet and supplements was associated with lower risks of PLC incidence and mortality in the US population. Magnesium intake from diet and supplements was evaluated through a food frequency questionnaire in a cohort of 104,025 participants. Cox regression was employed to calculate hazard ratios for PLC incidence and competing risk regression was employed to calculate subdistribution hazard ratios for PLC mortality. Restricted cubic spline regression was employed to test nonlinearity. We documented 116 PLC cases during 1,193,513.5 person-years of follow-up and 100 PLC deaths during 1,198,021.3 person-years of follow-up. Total (diet + supplements) magnesium intake was found to be inversely associated with risks of PLC incidence (hazard ratiotertile 3 vs. 1 : 0.44; 95% confidence interval: 0.24, 0.80; ptrend = 0.0065) and mortality (subdistribution hazard ratiotertile 3 vs. 1 : 0.37; 95% confidence interval: 0.19, 0.71; ptrend = 0.0008). Similar results were obtained for dietary magnesium intake. Nonlinear inverse dose-response associations with PLC incidence and mortality were observed for both total and dietary magnesium intakes (all pnonlinearity

The article analyzes properties of potassium and magnesium, which may exert vasodilatory, anti-inflammatory, anti-ischemic, antiaggregant, and antiarrhythmic effects. These are extremely important microelements and potentially beneficial therapeutic agents for treatment of cardiovascular diseases.

BACKGROUND The impact of admission serum magnesium on long-term mortality in hospitalized patients was unclear. This study aimed to assess the long-term mortality risk based on admission of serum magnesium in hospitalized patients. METHODS This was a retrospective cohort study conducted at a tertiary referral hospital. We included all adult patients admitted to Mayo Clinic Hospital, Minnesota, between 1 January 2009 and 31 December 2013, who had available admission serum magnesium. We categorized serum magnesium into ≤1.4, 1.5-1.6, 1.7-1.8, 1.9-2.0, 2.1-2.2, ≥2.3 mg/dL. We estimated the 1-year mortality risk based on various admission serum magnesium levels using Kaplan-Meier plot and assessed the association of admission serum magnesium with 1-year mortality using Cox proportional hazard analysis. We selected serum magnesium of 1.7-1.8 mg/dL as the reference group for mortality comparison. RESULTS We included a total of 65,974 patients, with a mean admission serum magnesium of 1.9 ± 0.3 mg/dL in this study. The 1-year mortality was 15.7%, 15.8%, 15.5%, 16.7%, 19.0%, and 25.6% in admission serum magnesium of ≤1.4, 1.5-1.6, 1.7-1.8, 1.9-2.0, 2.1-2.2, ≥2.3 mg/dL, respectively (p < 0.001). After adjustment for confounders, admission serum magnesium of 1.9-2.0, 2.1-2.2, and ≥2.3 mg/dL were significantly associated with increased 1-year mortality compared with magnesium of 1.7-1.8 mg/dL with adjusted HR of 1.09 (95% CI 1.02-1.15), 1.22 (95% CI 1.14-1.30), and 1.55 (95% CI 1.45-1.55), respectively. There was no significant difference in 1-year mortality risk between low serum magnesium ≤1.6 mg/dL and magnesium of 1.7-1.8 mg/dL. CONCLUSION Hypermagnesemia, but not hypomagnesemia, at the time of hospital admission was associated with increased 1-year mortality among hospitalized patients.

Many studies have confirmed the important roles of nutritional status and micronutrients in the COVID-19 pandemic. Magnesium is a vital essential trace element that is involved in oxidative stress, inflammation, and many other immunological functions and has been shown to be associated with the outcome of COVID-19 infection. Here, we conducted a nationwide retrospective cohort study in the United States involving 1150 counties, 287,326,503 individuals, and 5,401,483 COVID-19 confirmed cases as of 30 September 2020 to reveal the infection risk of the populations distributed in low-magnesium areas in the early transmission of COVID-19. Our results indicate that the average county-level COVID-19 cumulative incidence in low-magnesium areas was significantly higher than in the control areas. Additionally, a significant negative nonlinear association was found between environmental magnesium concentration and the county-level COVID-19 cumulative incidence. Furthermore, the populations distributed in low environmental magnesium areas faced a higher COVID-19 infection risk (RR: 1.066; CI: 1.063–1.068), among which females (RR: 1.07; CI: 1.067–1.073), the 0–17 years subgroup (RR: 1.125; CI: 1.117–1.134), the 65+ years subgroup (RR: 1.093; CI: 1.087–1.098), black people (RR: 1.975; CI: 1.963–1.986), populations outside metro areas, and counties with a smaller population experienced higher risk of infection by COVID-19 than other subgroups. Considering that the magnesium intake of about half the population of the United States is below the daily required dose, our study will contribute to the creation of long-term public health strategies to help protect against COVID-19.

An epileptic seizure is a common neurological presentation in the Emergency Department (ED). Electrolyte disturbances are an important cause of neurological symptoms like seizures and hypomagnesemia is one of them. PPI's can cause hypomagnesemia and are readily prescribed. Therefore patients taking PPI's are at risk of developing neurological symptoms due to hypomagnesemia.A 82-year old woman was seen in ED with a history of nausea, vomiting and vertigo. A vertical nystagmus was observed with attacks of mydriasis followed by a phase of encephalopathy and restlessness. These were recognized as epilepsy. Hypokaliemia, hypocalcemia and a deep hypomagnesemia were present. The PPI accounted for hypomagnesemia. After 2 days of intravenous magnesium suppletion all symptoms disappeared.PPI's can cause hypomagnesemia and magnesium levels should be obtained in patients presenting with encephalopathy or atypical neurological symptoms.

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.

Magnesium (Mg) is an essential metal for chlorophyll biosynthesis and other metabolic processes in plant cells. Mg is largely stored in the vacuole of various cell types and remobilized to meet cytoplasmic demand. However, the transport proteins responsible for mobilizing vacuolar Mg2+ remain unknown. Here, we identified two Arabidopsis (Arabidopsis thaliana) Mg2+ transporters (MAGNESIUM TRANSPORTER 1 and 2; MGT1 and MGT2) that facilitate Mg2+ mobilization from the vacuole, especially when external Mg supply is limited. In addition to a high degree of sequence similarity, MGT1 and MGT2 exhibited overlapping expression patterns in Arabidopsis tissues, implying functional redundancy. Indeed, the mgt1 mgt2 double mutant, but not mgt1 and mgt2 single mutants, showed exaggerated growth defects as compared to the wild type under low-Mg conditions, in accord with higher expression levels of Mg-starvation gene markers in the double mutant. However, overall Mg level was also higher in mgt1 mgt2, suggesting a defect in Mg2+ remobilization in response to Mg deficiency. Consistently, MGT1 and MGT2 localized to the tonoplast and rescued the yeast (Saccharomyces cerevisiae) mnr2Δ (manganese resistance 2) mutant strain lacking the vacuolar Mg2+ efflux transporter. In addition, disruption of MGT1 and MGT2 suppressed high-Mg sensitivity of calcineurin B-like 2 and 3 (cbl2 cbl3), a mutant defective in vacuolar Mg2+ sequestration, suggesting that vacuolar Mg2+ influx and efflux processes are antagonistic in a physiological context. We further crossed mgt1 mgt2 with mgt6, which lacks a plasma membrane MGT member involved in Mg2+ uptake, and found that the triple mutant was more sensitive to low-Mg conditions than either mgt1 mgt2 or mgt6. Hence, Mg2+ uptake (via MGT6) and vacuolar remobilization (through MGT1 and MGT2) work synergistically to achieve Mg2+ homeostasis in plants, especially under low-Mg supply in the environment.

Producción Científica, Magnesium (Mg) is an essential divalent cation involved in various enzymatic reactions that regulate vital biological functions. The main goal was to evaluate Mg status and its association with nutritional indicators in 78 children and adolescents with chronic diseases. We assessed an‐ thropometric, biochemical, diet, body composition, and bone densitometry valuations. Serum Mg and Ca levels were determined using the standardized method and diet calcium (Ca) and Mg con‐ sumption by a prospective 72 h diet survey. Mean serum Ca (9.9 mg/dL), Mg (2.08 mg/dL) dietary Ca (102% DRI: Dietary Reference Intake), and Mg intake (105% DRI) were normal. A total of 45% had hypomagnesemia, 12% had hypermagnesemia, and 26% and 24% had inadequate and high Mg intake, respectively. Only 6% of patients had poor Mg intake and hypomagnesemia, and 54% and 90% of our series had an elevated serum Ca/Mg ratio > 4.70 (mean 4.79) and a low Ca/Mg intake ratio < 1.70 (mean 1.06), respectively. Both Ca/Mg ratios were linked with the risk of developing other chronic conditions such as cardiovascular disease, type 2 diabetes, syndrome metabolic, and even several cancers. Therefore, 79% of children and adolescents with chronic diseases were at ele‐ vated risk of having abnormal Mg status and developing other chronic illnesses.

Introduction: The objective of this study was to review the current status of drug-induced hypomagnesemia and its adverse effects on cardiovascular disease (CVD) and hypertension. Since magnesium is a potent vasodilator, which modulates vasomotor tone, peripheral blood flow, and hypertension, its deficiency could have significant cardiovascular and blood pressure (BP) effects.Areas covered: Studies have shown that several factors can contribute to magnesium deficiency including age, diet, disease, and certain drugs such as diuretics and proton-pump inhibitors (PPIs). For an updated perspective of drug-induced hypomagnesemia, a Medline search of the English language literature was conducted between 2010 and 2019 using the terms diuretics, proton-pump inhibitors, hypomagnesemia, cardiovascular disease, hypertension, and 35 pertinent papers were retrieved.Expert opinion: The data showed that magnesium deficiency is difficult to occur since it is plentiful in green leafy vegetables, cereals, nuts, and the drinking water. However, magnesium deficiency can occur with the use of diuretics for the treatment of hypertension and heart failure, or the use of PPIs for the treatment of gastroesophageal reflux disease. Therefore, magnesium deficiency should be detected and treated to prevent the aggravation of hypertension and the onset of CVD and serious cardiac arrhythmias including torsades de points.

X-linked immunodeficiency with magnesium defect, EBV infection, and neoplasia (XMEN) disease are caused by deficiency of the magnesium transporter 1 (MAGT1) gene. We studied 23 patients with XMEN, 8 of whom were EBV naive. We observed lymphadenopathy (LAD), cytopenias, liver disease, cavum septum pellucidum (CSP), and increased CD4-CD8-B220-TCRαβ+ T cells (αβDNTs), in addition to the previously described features of an inverted CD4/CD8 ratio, CD4+ T lymphocytopenia, increased B cells, dysgammaglobulinemia, and decreased expression of the natural killer group 2, member D (NKG2D) receptor. EBV-associated B cell malignancies occurred frequently in EBV-infected patients. We studied patients with XMEN and patients with autoimmune lymphoproliferative syndrome (ALPS) by deep immunophenotyping (32 immune markers) using time-of-flight mass cytometry (CyTOF). Our analysis revealed that the abundance of 2 populations of naive B cells (CD20+CD27-CD22+IgM+HLA-DR+CXCR5+CXCR4++CD10+CD38+ and CD20+CD27-CD22+IgM+HLA-DR+CXCR5+CXCR4+CD10-CD38-) could differentially classify XMEN, ALPS, and healthy individuals. We also performed glycoproteomics analysis on T lymphocytes and show that XMEN disease is a congenital disorder of glycosylation that affects a restricted subset of glycoproteins. Transfection of MAGT1 mRNA enabled us to rescue proteins with defective glycosylation. Together, these data provide new clinical and pathophysiological foundations with important ramifications for the diagnosis and treatment of XMEN disease.

Contains fulltext : 215418.pdf (Publisher’s version ) (Closed access) BACKGROUND: Hypomagnesemia has been associated with diabetes, cardiovascular disease, and other disorders. Drug use has been suggested as one of the risk factors for low magnesium (Mg) levels. In the elderly population, prone to polypharmacy and inadequate Mg intake, hypomagnesemia might be relevant. Therefore, we aimed to investigate associations between drug use and plasma Mg. METHODS: Cross-sectional data of 343 Dutch geriatric outpatients were analysed by Cox and linear regression, while adjusting for covariates. Drug groups were coded according to the Anatomical Therapeutic Chemical classification system; use was compared to non-use. Hypomagnesemia was defined as plasma Mg < 0.75 mmol/l and /=5 medications (polypharmacy). The number of different drugs used was inversely linearly associated with Mg level (beta -0.01; p < 0.01). Fully adjusted Cox regression showed significant associations of polypharmacy with hypomagnesemia (Mg < 0.75 mmol/l) (prevalence ratio (PR) 1.81; 95%CI 1.08-3.14), proton pump inhibitors (PR 1.80; 95%CI 1.20-2.72), and metformin (PR 2.34; 95%CI 1.56-3.50). Moreover, stratified analyses pointed towards associations with calcium supplements (PR 2.26; 95%CI 1.20-4.26), insulins (PR 3.88; 95%CI 2.19-6.86), vitamin K antagonists (PR 2.01; 95%CI 1.05-3.85), statins (PR 2.44; 95%CI 1.31-4.56), and bisphosphonates (PR 2.97; 95%CI 1.65-5.36) in patients

Magnesium (Mg) is the second most abundant intracellular cation and plays a significant role in immune system and cardiac protection. Mg deficiency contributes to chronic low-grade inflammation leading to cardiovascular diseases, and low Mg level exacerbates virus-induced inflammation. The aim of the study was to investigate whether serum magnesium level is associated with myocardial damage and prognosis of COVID-19. This was a single-center, observational retrospective study of patients with COVID-19. The study population was divided into two groups according to in-hospital mortality: a survivor group (SG) and a non-survivor group (NSG). Myocardial damage was defined as blood levels of cardiac troponin I (cTnI) above the 99

Oxidative stress which refers to redox imbalance with increased generation of reactive oxygen species (ROS) has been associated with the pathophysiology of diverse disease conditions. Recently, a close, yet not fully understood, relation between oxidative stress and neuropeptides, in particular, substance P (SP), has been reported in certain conditions. SP has been shown to affect the cellular redox environment through activation of neurokinin-1receptor (NK1R). It seems that SP/NK1R system and oxidative stress can act either synergistically or antagonistically in a context-dependent manner, thereby, influencing the pathology of various clinical disorders either destructively or protectively. Importantly, the interactions between oxidative stress and SP/NK1R system can be pharmacologically targeted. Therefore, a better understanding of the redox modulatory properties of SP/NK1R signaling will pave the way for identifying new therapeutic possibilities for attenuating oxidative stress-mediated damage. Towards this end, we performed a comprehensive search through PubMed/Medline and Scopus databases and discussed all related existing literature regarding the interplay between oxidative stress and SP/NK1R system as well as their implication in various clinical disorders, to provide a clear view and hence better management of oxidative damage.

The aim of the study was to evaluate the significance of hypomagnesemia in patients with coronavirus disease 2019 (COVID-19) and clarify its possible pathogenesis. A retrospective cohort study was conducted by reviewing 83 patients hospitalized in Guanggu district, Wuhan Third Hospital, China. Clinical histories, laboratory findings and outcome data were collected. Eighteen patients had hypomagnesemia during hospitalization. Fourteen patients were in the critical group and six died. In the critical group, serum magnesium (0.72 ± 0.15 mmol/L) was much lower than that in the moderate and severe groups. At the same time, we also found that several indicators are correlated with the level of magnesium. The level of magnesium was positively associated with the lymphocyte count (r = 0.203, P = 0.004) and platelet count (r = 0.217, P = 0.002) but negatively related to the levels of CRP (r = -0.277, P = 0.000), LDH (r = -0.185, P = 0.011) and α-hydroxybutyrate dehydrogenase (r = -0.198, P = 0.008) in the critical group. Hypomagnesemia might increase symptoms and may be associated with mortality in COVID-19 by affecting enzyme activity and activating the inflammatory response. Thus, magnesium might play a key role in the pathogenesis of COVID-19.

This study aimed to determine the relationship between hospital-acquired dysmagnesemia and in-hospital mortality in critically ill patients. A retrospective cohort study was conducted on critically ill patients who had normal serum magnesium levels on admission. Data were extracted from the Multiparameter Intelligent Monitoring in Intensive Care III database. The normal range of serum magnesium was 1.6-2.6 mg/dL. In-hospital serum magnesium levels were categorized based on the occurrence of hospital-acquired hypomagnesemia and hypermagnesemia. Hospital-acquired hypomagnesemia and hypermagnesemia in the same patient were defined as a patient with the lowest level of serum magnesium of1.6 mg/dL and the highest level of serum magnesium of2.6 mg/dL, respectively. The in-hospital outcomes were collected. The findings revealed that 27.2% of patients developed hospital-acquired dysmagnesemia. In-hospital mortalities were 8.8% in patients with persistently normal serum magnesium levels, 12.2% in patients with hospital-acquired hypomagnesemia only, 18.4% in patients with hospital-acquired hypermagnesemia only, and 20.6% in patients with both hospital-acquired hypomagnesemia and hypermagnesemia. Compared to patients with persistently normal serum magnesium in hospital, those with hospital-acquired hypermagnesemia only [odds ratio (OR) = 1.346, P 0.001] and those with both hospital-acquired hypomagnesemia and hypermagnesemia (OR = 1.333, P = 0.001) were significantly associated with higher in-hospital mortality. Hospital-acquired dysmagnesemia was common among critically ill patients. Hospital-acquired dysmagnesemia, especially hospital-acquired hypermagnesemia, was significantly associated with increased in-hospital mortality in critically ill patients.

Magnesium deficiency can have serious health consequences. Low magnesium intake or low serum levels are risk factors for e.g. type 2 diabetes and cardiovascular diseases. Despite its scientifically recognized importance, too little attention is paid to magnesium in clinical practice. This may be due to the fact that there is no uniform and evidence-based reference range for serum magnesium as is the case for other electrolytes such as sodium and potassium. The serum magnesium concentration is also of a limited informative value, as it is maintained for a long time by releasing magnesium from body pools. A low serum magnesium is a definite sign of magnesium deficiency; however, values within the reference range do not rule out deficiencies. Nevertheless, serum magnesium should become part of routine diagnostics in order to be able to better detect deficiency states. For serum magnesium, a reference range of 0.75 to 0.95 mmol/L (1.82 to 2.31 mg/dL) can often be found. However, according to the current data situation, serum magnesium values of less than 0.85 mmol/L are associated with increased health risks. Therefore, the lower limit of the reference range should be raised to 0.85 mmol/L (2.07 mg/dL).

The elderly are at great risk of developing life-threatening disturbances in calcium–magnesium–phosphate homeostasis because of comorbidities, long-term medication use, and dietary deficiencies, but it is still not known how often they occur in this group of patients. This study aimed to assess the prevalence of these disturbances in a group of hospitalized patients over 65 years of age according to age and sex. The study was conducted between January 2018 and September 2020 at the Central Clinical Hospital in Warsaw. A total of 66,450 calcium, magnesium, phosphate, and vitamin D concentration results were included in the analysis. Dysmagnesemia was present in 33% of the calcium results, dyscalcemia, dysphosphatemia, and dysvitaminosis D—in 23.5%, 26%, and 70% of the results, respectively. The magnesium concentration was found to be age-dependent, and older people were found to be at higher risk of developing abnormal magnesium concentrations (p &lt, 0.001). Sex influenced the occurrence of abnormal magnesium (p &lt, 0.001), vitamin D (p &lt, 0.001), and calcium (p &lt, 0.00001) concentrations, with hypercalcemia and hypervitaminosis D disorders being significantly more common in women (p &lt, 0.0001). In conclusion, disorders of the calcium–magnesium–phosphate metabolism are common in hospitalized patients over 65 years of age, and the concentrations of these substances should be routinely monitored in this group.

So far, there is no consistent and convincing theory explaining the pathogenesis of migraines. Vascular disorders, the effect of oxidative stress on neurons, and the contribution of magnesium-calcium deficiencies in triggering cortical depression and abnormal glutaminergic neurotransmission are taken into account. However, there are no reliable publications confirming the role of dietary deficits of magnesium and latent tetany as factors triggering migraine attacks. The aim of the study was to evaluate the influence of latent magnesium deficiency assessed with the electrophysiological tetany test on the course of migraine. The study included: a group of 35 patients (29 women and six men, in mean age 41 years) with migraine and a control group of 24 (17 women and seven men, in mean age 39 years) healthy volunteers. Migraine diagnosis was based on the International Headache Society criteria, 3rd edition. All patients and controls after full general and neurological examination were subjected to a standard electrophysiological ischemic tetany test. Moreover, the level of magnesium in blood serum was tested and was in the normal range in all patients. Then, the incidence of a positive tetany EMG test results in the migraine group and the results in the subgroups with and without aura were compared to the results in the control group. Moreover, the relationship between clinical markers of spasmophilia and the results of the tetany test was investigated in the migraine group. As well as the relationship between migraine frequency and tetany test results. There was no statistically significant difference in the occurrence of the electrophysiological exponent of spasmophilia between the migraine and control group. Neither correlation between the occurrence of clinical symptoms nor the frequency of migraine attacks and the results of the tetany test was stated (p &gt, 0.05). However, there was an apparent statistical difference between the subgroup of migraine patients with aura in relation to the control group (p &lt, 0.05). The result raises hope to find a trigger for migraine attacks of this clinical form, the more that this factor may turn out to be easy to supplement with dietary supplementation.

Magnesium (Mg) is commonly addressed as the “forgotten ion” in medicine. Nonetheless, hypomagnesemia should be suspected in clinical practice in patients with relevant symptomatology and also be considered a predisposing factor for the development of other electrolyte disturbances. Furthermore, chronic hypomagnesemia has been associated with diabetes mellitus and cardiovascular disease. Hypomagnesemia as a consequence of drug therapy is relatively common, with the list of drugs inducing low serum Mg levels expanding. Culprit medications linked to hypomagnesemia include antibiotics (e.g. aminoglycosides, amphotericin B), diuretics, antineoplastic drugs (cisplatin and cetuximab), calcineurin inhibitors, and proton pump inhibitors. In recent years, the mechanisms of drug‐induced hypomagnesemia have been unraveled through the discovery of key Mg transporters in the gut and kidney. This narrative review of available literature focuses on the pathogenetic mechanisms underlying drug‐induced hypomagnesemia in order to increase the insight of clinicians toward early diagnosis and effective management.