Oral Magnesium Supplementation Research Articles

A study on the impact of Magnesium on the Glycemic regulation

Objectives: The present study was to evaluate the impact of magnesium on glycemic regulation and also evaluate the changes of glycemic control indicators in type 2 diabetes mellitus patients. Methods: A total of 50 subjects aged 30–60 years with the FBS of more than 126 mg/dL who had been recently diagnosed with T2D (maximum one year) and were being treated with antidiabetic drugs were enrolled in the present study. All the subjects were instructed to follow a prescribed diet plan for one week to stabilize their serum glucose level (30% of total energy as fat, 15% of energy as protein, and 55% of energy as carbohydrate-focused, from complex carbohydrates). Both groups were instructed to consume a healthy diet of fruits and vegetables (five serving per day), legumes, nuts and whole grains. The intervention group consisted of 25 participants who were on Mg supplementation for three months. The control group (25 participants) were not received any type of supplement throughout the intervention period. Body weight and height were measured to calculate body mass index (BMI). All measurements and indicators were taken at the base line (Pre) and after three months of intervention (post changes). Results: Mean age group of intervention and control group was not significant (p=0.118). In both group, males were more preponderance than females. When we compared the mean BMI, HbA1C, C-peptide (ng/mL), HOMA.?%, and Mg (mg/dL) between intervention and control group subjects respectively. P-value was found to be 0.512, 0.588, 0.117, 0.606, 0.317, and 0.235 respectively. Mean FBS of interventional group patients was significantly (p=0.011) reduced in post intervention as compared to pre intervention. While in control group, mean FBS was not significant differences (p=0.184). Mean Ca of interventional group subjects was extreme significantly (p<0.0001) decreased in post intervention as compared to preintervention. While in control group subjects, mean Ca was not significantly decreased in post-test as compared to pre-test. In interventional group subjects, mean Mg was highly significantly (p=002) increased in post intervention as compared to pre intervention. While in control group subjects, mean Mg level was extreme significantly (p<0.0001) reduced in post-test as compared to pre-test. Conclusions: Oral magnesium supplement significantly decreases the fasting blood sugar level. And it reduces the insulin resistance and improves the glycaemic control indicators in type 2 diabetes mellitus patients. Key words: Magnesium, glycaemic control indicators, type 2 diabetes mellitus.

Intestinal Oxalate Absorption, Enteric Hyperoxaluria, and Risk of Urinary Stone Formation in Patients with Crohn's Disease.

Nephrolithiasis is a common urologic manifestation of Crohn's disease. The purpose of this study was to investigate the clinical characteristics, intestinal oxalate absorption, and risk factors for urinary stone formation in these patients. In total, 27 patients with Crohn's disease and 27 healthy subjects were included in the present study. Anthropometric, clinical, and 24 h urinary parameters were determined, and the [13C2]oxalate absorption test was performed. Among all patients, 18 had undergone ileal resection, 9 of whom had a history of urinary stones. Compared to healthy controls, the urinary excretion values of calcium, magnesium, potassium, sulfate, creatinine, and citrate were significantly lower in patients with Crohn's disease. Intestinal oxalate absorption, the fractional and 24 h urinary oxalate excretion, and the risk of calcium oxalate stone formation were significantly higher in patients with urolithiasis than in patients without urolithiasis or in healthy controls. Regardless of the group, between 83% and 96% of the [13C2]oxalate was detected in the urine within the first 12 h after ingestion. The length of ileum resection correlated significantly with the intestinal absorption and urinary excretion of oxalate. These findings suggest that enteric hyperoxaluria can be attributed to the hyperabsorption of oxalate following extensive ileal resection. Oral supplementation of calcium and magnesium, as well as alkali citrate therapy, should be considered as treatment options for urolithiasis.

How much magnesium sulfate is needed to "keep total serum magnesium above 2.0 mg/dL"?

For patients at increased risk of life-threating ventricular arrythmias, hospitalists often administer intravenous magnesium sulfate to maintain total serum magnesium concentration (TsMg) above 2 mg/dL. How long each dose keeps TsMg above this threshold is not well known, however. We collected TsMg values from 12,618 veterans who were given 24,363 doses of intravenous magnesium sulfate during 14,901 hospitalizations for acute heart failure. Across dose amounts, the average TsMg dropped below 2.0 mg/dL within 24 h of administration. When we limited our analysis to 2 g doses (the most common dose) and adjusted for baseline TsMg, estimated glomerular filtration rate, oral magnesium supplementation, and loop diuretic dosing, we found that less than half of the adjusted TsMg values remained above 2.0 mg/dL just 12 h after dose administration. Hospitalists should expect, on average, to administer 2 g intravenous magnesium sulfate at least twice daily to maintain total serum magnesium above 2 mg/dL.

Oral magnesium supplementation does not affect insulin sensitivity in people with insulin-treated type 2 diabetes and a low serum magnesium: a randomised controlled trial

Aims/hypothesisHypomagnesaemia has been associated with insulin resistance and an increased risk of type 2 diabetes. Whether magnesium supplementation improves insulin sensitivity in people with type 2 diabetes and a low serum magnesium level is unknown.MethodsUsing a randomised, double-blind (both participants and investigators were blinded to the participants’ treatment sequences), placebo-controlled, crossover study design, we compared the effect of oral magnesium supplementation (15 mmol/day) for 6 weeks with that of matched placebo in individuals with insulin-treated type 2 diabetes (age ≥18 years, BMI 18–40 kg/m2, HbA1c <100 mmol/mol [11.3%], serum magnesium ≤0.79 mmol/l). Participants were recruited from the outpatient clinic and through advertisements. Randomisation to a treatment sequence order was done using a randomisation list. We used block randomisation and the two possible treatment sequences were evenly distributed among the trial population. The primary outcome was the mean glucose infusion rate during the final 30 min of a hyperinsulinaemic–euglycaemic clamp (i.e. M value). Secondary outcomes included variables of glucose control, insulin need, BP, lipid profile and hypomagnesaemia-related symptoms during follow-up.ResultsWe recruited 14 participants (50% women, 100% White, mean ± SD age 67±6 years, BMI 31±5 kg/m2, HbA1c 58±9 mmol/mol [7.4±0.9%]) with insulin-treated type 2 diabetes. Magnesium supplementation increased both mean ± SEM serum magnesium level (0.75±0.02 vs 0.70±0.02 mmol/l, p=0.016) and urinary magnesium excretion (magnesium/creatinine ratio, 0.23±0.02 vs 0.15±0.02, p=0.005), as compared with placebo. The M value of the glucose clamp did not differ between the magnesium and placebo study arms (4.6±0.5 vs 4.4±0.6 mg kg−1 min−1, p=0.108). During the 6 weeks of treatment, continuous glucose monitoring outcomes, HbA1c, insulin dose, lipid profile and BP also did not differ, except for a lower HDL-cholesterol concentration after magnesium compared with placebo (1.14±0.08 vs 1.20±0.09 mmol/l, p=0.026). Symptoms potentially related to hypomagnesaemia were similar for both treatment arms.Conclusions/interpretationDespite an albeit modest increase in serum magnesium concentration, oral magnesium supplementation does not improve insulin sensitivity in people with insulin-treated type 2 diabetes and low magnesium levels.Trial registrationEudraCT number 2021-001243-27.FundingThis study was supported by a grant from the Dutch Diabetes Research Foundation (2017–81–014).Graphical

Abstract #1408162: Comparison of Different Doses of Sodium-Glucose Ttransporter-2 Inhibitors (SGLT2i) to SGLT2i with Magnesium Infusions for Refractory Hypomagnesaemia in a Patient with Monogenic Diabetes Type-5 (MODY-5)

MODY-5 is a rare autosomal dominant form of monogenic diabetes attributed to deletions of chromosome 17q12 with impaired expression of HNF1β (Hepatocyte Nuclear Factor 1 homeobox Beta. The deficient HNF1B down regulated the expression of FXYD2. Refractory hypomagnesemia is commonly observed in patients with MODY-5 due to downregulated FXYD2 which blocked the encoding of the γ (gamma) subunit of the Na+-K+-ATPase and indirectly led to hypomagnesemia. SGLT2i have been associated with small but significant increases in serum magnesium (sMg) levels in patients with diabetes. We report our patient's experience comparing the use of SGLT2i at different doses to SGLT2i with Mg infusions for refractory hypomagnesemia in a patient with MODY-5. 29 y/o Caucasian female with family history of young onset diabetes was diagnosed with MODY-5 at the age of 19 years old when she was found to have kidney cysts that were noted incidentally on MRI spine. She presents to our clinic with hypertension, catamenial headaches, hyperuricemia, refractory hypomagnesemia to oral magnesium supplements (400mg twice a day) due to Mg wasting syndrome, congenital pancreatic atresia and exocrine pancreatic insufficiency. sMg levels have been <1.0mg/dl for 2 years and was symptomatic due to it such as fatigue, headaches and muscle aches. Most lately, she could not tolerate more than 1000mg twice a day of oral magnesium due to diarrhea. Prior to starting SGLT2i her sMg was <1.0mg/dl and fractional excretion of magnesium (FEMg) was 14.5% (normal FEMg <4% in the setting of hypomagnesemia). She was started on canagliflozin 100mg and was titrated to 300mg; which has improved her sMg level from 0.9 mg/dl to 1.2mg/dl and was stable with this dose for weeks. FEMg data was not available for the dose change of canagliflozin. She was also started on amiloride 5mg daily. sMg levels have dropped to <1 md/dL when the canagliflozin has been stopped due to insurance but improved again after starting empagliflozin. On 10mg of empagliflozin compared to 25mg of empagliflozin the sMg level has not changed and remained at 1.1mg/dl level but the FEMg improved from 10% to 7.25%. She continued to have symptoms of hypomagnesemia, so she was started on magnesium sulfate 2gm in 100ml normal saline infused over 12hrs 3 times a week for 6 months. Her symptoms improved after the infusion, but they wear off quickly. Magnesium infusions improved the sMg to 1.5mg/dl but the FEMg was 12.6%. Did not improve. Lately due to treatment burden of Magnesium infusion, they were decreased to 2 times per week. SGLT2i improve refractory hypomagnesemia due to Mg wasting syndrome. Her sMg improved to >1 mg/dL with SGLT2i. There was no difference in sMg comparing low versus high doses of empagliflozin, but an improvement in FEMg. Adding magnesium infusion to SGLT2i slightly improved sMg, but at the expense of burden of the disease treatment.

COMPARATIVE ANALYSIS OF SERUM MAGNESIUM &amp; ZINC LEVELS AND THEIR ASSOCIATIONS WITH PRETERM LABOUR

Background: Preterm is dened as babies born alive before 37 weeks of pregnanc, it occurs when there is a regular contraction of uterus which results in opening of cervix after 20 weeks and before 37 weeks of gestation. preterm labour is spontaneous but it can also be due to a biochemical changes in body functions at the cellular level of trace elements such as magnesium and zinc. The main objective of this study is to nd the association of hypomagnesaemia and low zinc levels in preterm delivered women and to compare the maternal serum magnesium and zinc levels between Preterm and Term delivered mothers. Methods: A Comparative study was done in the Department of Biochemistry, Andhra Medical College, Visakhapatnam. Atotal of 126 women who were admitted to the labour room at Department of Obstetrics and gynaecology, King George Hospital, Visakhapatnam were selected for this study. All the subjects were divided into two groups as Preterm Consists of 63 women with spontaneous preterm labour delivered between 28- 37 weeks and Term Consists of 63 Women with Term labour after 37 weeks. Results: Women with Preterm labour had a signicantly low serum magnesium level with a mean serum magnesium level of 1.8 mg/dl with SD of 0.38 whereas the patients with Term labour had a mean serum magnesium level of 2.09 mg/dl with SD of 0.50 and also low zinc levels in Preterm labour with mean zinc levels of 51.28 µg/dl with SD 10.9 whereas patients with Term labour had mean serum zinc levels of 56.5 µg/dl with SD 9.7. The difference of serum magnesium and zinc levels observed between the study population and control population is independent of factors like maternal age, parity, gestational age, Blood pressure and socioeconomic status. In this study there is non signicant weak correlation was found between Demographic data and parametric data. Conclusions:Serum magnesium and zinc levels can be used as predictors for preterm labour. Spontaneous preterm delivery can be avoided by early assessment of maternal magnesium and zinc status and also by simple oral supplementation of magnesium and zinc which might provide an easy and inexpensive means to decrease the problems related to preterm labour. There is a further scope for research on serum magnesium and zinc levels based on gestational age.

The Effect of Oral Magnesium Supplement on Pre-eclampsia and Perinatal Outcomes in Pregnancy: A Meta-Analysis of Randomized Controlled Trials

Background: Magnesium is one of the most important nutritional factors that have a beneficial effect on pregnant women. Many studies evaluated the role of oral magnesium supplements as a non-pharmacological intervention for mother and neonatal protection in terms of these outcomes. There is a conflict between several clinical trials about the efficacy of oral magnesium supplements during pregnancy. Therefore, in this review, we represent class 1 evidence and address an unmet clinical need on the efficacy of different types of oral magnesium in pre-eclampsia, and prenatal outcomes in pregnant women.&#x0D; Method: During the preparation of this meta-analysis, we followed the PRISMA statement guidelines. A literature search of the Web of Sciences, Cochrane Central Register of Controlled Trials, and PubMed were conducted from inception until September 2022. We included randomized controlled trials (RCTs) comparing oral magnesium whether citrate, oxide, or aspartate hydrochloride with a placebo. The records of quality studies were screened and extracted. Additionally, the pre-eclampsia, preterm birth, and neonatal intensive care unit (NICU) admissions data were pooled as odds ratio (OR) in a fixed-effect model using Review Manager (v.3). Subgroup analysis was performed to investigate the efficacy of each type of oral magnesium on the outcomes.&#x0D; Results: Five RCTs were included in this meta-analysis with a total of 2370 patients. The overall effect did not favor either of the two groups in terms of pre-eclampsia (OR= 0.99, 95% CI, [0.72, 1.37], p = 0.9), preterm birth (OR= 0.87, 95% CI, [0.62, 1.22], p = 0.4), and NICU admissions (OR= 1.37, 95% CI, [0.84, 2.22], p = 0.2). Based on the subgroup analysis findings, the use of oral magnesium supplements whether citrate, oxide, or aspartate hydrochloride in this population did not significantly increase or decrease the incidence of pre-eclampsia, preterm birth, and NICU admissions when compared with the control group.&#x0D; Conclusion: Ultimately, oral magnesium supplementation whether citrate, oxide, or aspartate hydrochloride may not have a beneficial effect on maternal and fetal outcomes during pregnancy. Therefore, the current evidence is insufficient to confirm the efficacy of oral magnesium for care practice among pregnant women. Despite that, these results need to be affirmed by major RCTs using magnesium supplements which have related to neonatal and maternal outcomes.

Hypomagnesemia as a Risk Factor and Accelerator for Vascular Aging in Diabetes Mellitus and Chronic Kidney Disease.

The age-old axiom that one is as old as his or her vessels are, calls for ongoing critical re-examination of modifiable risk factors of accelerated vascular ageing in chronic kidney diseases. Attempts to modulate vascular risk with cholesterol-lowering agents have largely failed in advanced chronic kidney disease (CKD). In addition to nitrogen waste products, many pathological biochemical processes also play a role in vascular calcification in chronic kidney damage. Magnesium, a cation vital for the body, may substantially reduce cardiovascular diseases' risk and progression. This narrative review aimed to address the relationship between hypomagnesemia and vascular calcification, which promotes further cardiovascular complications in diabetes, aging, and CKD. Articles with predefined keywords were searched for in the PubMed and Google Scholar databases with specific inclusion and exclusion criteria. We hypothesized that a decrease in serum magnesium levels contributes to increased vascular calcification and thereby increases cardiovascular mortality. In summary, based on existing evidence in the literature, it appears that simple and inexpensive oral magnesium supplementation may reduce the cardiovascular mortality of patients who are already severely affected by such diseases; in this context, the concept of 'normal' vs. 'ideal' serum magnesium levels should be carefully re-examined.

Preispitivanje uloge magnezijuma u istraživanjima epilepsije i zbrinjavanju pacijenata sa epilepsijom

Magnesium is a bioessential mineral with multiple neuroactive effects. Mg2+ ion stabilizes excitable membranes. Epilepsy is the third most frequent chronic neurological condition characterized by spontaneous reappearance of unprovoked epileptic seizures, whose underlying mechanisms are not completely understood yet. A literature review on the role of magnesium in basic and clinical epileptology has been made in order to enlighten the importance of magnesium deficiency in the mechanisms of epileptic brain hyperexcitability, as well as the significance of including magnesium into the management of epilepsy patients. Neuronal magnesium requirements are high. The concentration of magnesium in the cerebrospinal fluid (CSF) is even higher than in the blood. In experimental epilepsy research, perfusing hippocampal slices with artificial CSF containing low concentration of extracellular Mg2+ is a frequently used animal model of spontaneously induced epileptiform activity. Magnesium deficiency is the most frequent clinically unrecognized electrolyte disbalance, often overlooked in epilepsy patients. Serum and CSF Mg2+ concentrations are lower in patients with epilepsy, as compared to healthy controls. Hypomagnesaemia increases seizure frequency and the risk of sudden unexpected death in pharmacoresistant epilepsy. Oral magnesium supplements help achieve better seizure control. Parenterally administered Mg2+ efficiently controls seizures in several epileptic encephalopathies in adults and children (in eclampsia, uremia, porphyria, febrile seizures, infantile spasms), and also helps control status epilepticus. Subclinical magnesium deficiency, very frequent in general population, acts as a factor contributing to seizure generation in epilepsy. It is recommended to assess magnesium status in epilepsy patients. This literature review reveals the therapeutic potential of magnesium as a simple antiepileptic agent, which exceeds its current clinical use.

Author Correction: Oral supplementation of α-lipoic acid (ALA), magnesium, vitamin B6 and vitamin D stabilizes cervical changes in women presenting risk factors for preterm birth.

Correction to: European Review for Medical and Pharmacological Sciences 2022; 26 (23): 8879-8886. DOI: 10.26355/eurrev_202212_30560-PMID: 36524507-published online on December 15, 2022. After publication, the authors found out that in Figure 1 a box, including 63 patients included in the final analysis was missing. There are amendments to this paper. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/30560.

Oral supplementation of α-lipoic acid (ALA), magnesium, vitamin B6 and vitamin D stabilizes cervical changes in women presenting risk factors for preterm birth.

Recently, the PTB risk has been related to the objective measurement of cervical length (CL), since a CL of less than 25 mm is an accurate predictor of increased risk of PTB. Primary prevention of preterm labor is based on the early identification of symptoms and on pharmacological treatments with tocolytic drugs for inhibition of uterine contractions that are associated with a shortening of the cervix. Unfortunately, most of these drugs have important side effects. This study aimed to evaluate whether the administration of a combination of oral α-lipoic acid (ALA), magnesium, vitamin B6 and vitamin D to pregnant women presenting risk factors for PTB could reduce the rate of cervical shortening at 19-22 weeks of gestational age. A total of 122 women attending the first-trimester aneuploidy screening at 11-14 weeks of pregnancy and presenting risk factors for PTB were included in the study. Cervical length significantly decreased in the control group compared with the treatment group (-3.86 ± 1.97 vs. 1.50 ± 1.26; p=0.02). Although the rate of preterm birth did not significantly decrease (9.5% vs. 5.1%), admission for threatened PTB was statistically reduced in the treatment group compared with the control group (3.4% vs. 14.3%). Oral supplementation of ALA, magnesium, vitamin B6 and vitamin D significantly counteracted cervix shortening in pregnant women presenting risk factors for PTB.

Highly Efficient & Specific Repair of MAGT1 Mutation in Xmen Patient T Cells and Hematopoietic Stem Cells

Introduction: X-linked immunodeficiency with magnesium defect, Epstein-Barr virus (EBV) infection, and neoplasia (XMEN) is a congenital glycosylation disorder with combined immune deficiency due to Magnesium Transporter 1 (MAGT1) mutations. Defective glycosylation of Natural Killer Group 2D (NKG2D), an activating receptor expressed on CD8 and NK cells critical for cytotoxicity, results in EBV lymphoproliferative disease and an inverted CD4:CD8 ratio in many XMEN patients. Oral magnesium supplementation for XMEN patients was not helpful, and hematopoietic stem cell transplants (HSCT) are complicated by high mortality. CRISPR-Cas9-AAV inserts MAGT1 specifically at endogenous locus but relies on double strand DNA breaks and adeno-associated virus donor that triggers DNA damage response. To address this, we evaluated base editing approach to repair a MAGT1 mutation that affects multiple patients with XMEN disease. We observed highly efficient mutation repair of XMEN T cells (75.5%) and hematopoietic stem cells (71.9%) to restore MAGT1 function and persistence of gene correction following transplant into immunodeficient mice. Materials and methods: Peripheral blood hematopoietic stem cells (HSPCs, CD34+) and mononuclear cells (PBMC) were collected from XMEN patients and healthy donors (HD) after G-CSF and plerixafor mobilization. PBMCs were stimulated (anti-CD3/anti-CD28, IL-2 (100 IU/mL), in ImmunoCult™-XF T cell expansion medium for 5-7 days prior to editing. HSPCs were cultured in StemSpan™ SFEM II Stem Cell Factor, Thrombopoietin, Fms-like tyrosine kinase 3 ligand (all 100ng/mL) and UM171 for two days prior to editing. Base editing is performed by electroporation (MaxCyte Inc.) of cells with ABE8e SpRY (CELLSCRIPT LLC.) and synthetic guide (Synthego) RNAs. For in vitro killing activity, T cells were co-cultured with EBV-B cells at a ratio of 1:1 for 48 hours and analyzed for apoptosis (Apoptracker Green+ 7AAD-), necrosis (Apoptracker Green+ 7AAD+) and degranulation (CD8+ CD107a+). HSPCs were transplanted into mice two days after EP and harvested 17-20 weeks after transplant. Results:Base editing of XMEN T cells: Flow cytometric analysis 2 days post BE show restored expression of biomarker NKG2D in XMEN CD8+ T cells (75.5%) compared to HD (93.2%) and naïve XMEN (2.39%). CD8+ cytotoxic activity against EBV-B cells was restored in BE XMEN patient cells; as indicated by increased apoptosis (BE: 6.78%, naïve: 4.82%, HD: 8.17%), necrosis (BE: 9.35%, naïve: 4.54%, HD: 7.19%), and degranulation (BE: 22.80%, naïve: 15.50%, HD: 21.40%), compared to naïve MAGT1 CD8+ T cells.In an in vivo tumor model, BE XMEN T cells injected into mice with induced luminescent EBV-B cell tumors lysed tumors and reduced average bioluminescence flux (photons/sec) (7 weeks) (8.23 × 107 ± 1.06 × 108) compared to naïve T cells (3.39 × 109 ± 2.22 × 109 and HD T cells (1.45 × 109 ± 2.22 × 109). Base editing of HSPCs: Immunodeficient NSGS pups transplanted with BE XMEN HSPCs engrafted and differentiated normally into lymphocytes with a normalized CD4:CD8 ratio in spleen (BE: 0.79 ± 0.14, naïve: 3.45 ± 1.1, HD: 1.3 ± 0.40) and peripheral blood (BE: 2.16 ± 0.84, naïve: 5.56 ± 2.32, HD: 1.79 ± 0.70) (Fig 1a). Importantly, restoration of biomarker NKG2D expression selectively on CD8+ T cells in spleen (BE: 80.5% ± 8.61%, naïve: 3.63% ± 1.45%, HD: 68.9% ± 10.32%) and peripheral blood (BE: 86.1% ± 2.88%, naïve: 2.25% ± 1.45%, HD: 62.6% ± 12.44%) (Fig 1b) confirmed correction of MAGT1 function in the glycosylation of critical NKG2D protein. High throughput targeted sequencing of on-target locus shows minimal bystander edits and additional off-target analysis is ongoing. Conclusion: Our data show highly efficient and specific base editing repair of MAGT1 mutation in XMEN T lymphocytes and CD34+ HSPCs. BE XMEN T cells increased cytotoxic activity in vitro and killing of tumor cells in mice. In vivo studies with mice transplanted with BE CD34+ HSPCs also confirm long term engraftment and differentiation into CD8+ T cells with restored NKG2D necessary for activation and cytolytic activity of CD8+ T and NK cells. The highly efficient and specific correction with base editing holds great promise for gene therapy for XMEN disease. Figure 1View largeDownload PPTFigure 1View largeDownload PPT Close modal

Beneficial effects of adding magnesium to desalinated drinking water on metabolic and insulin resistance parameters among patients with type 2 diabetes mellitus: a randomized controlled clinical trial

There is evidence that increasing the consumption of water containing magnesium can improve glucose metabolism and insulin resistance in patients with type 2 diabetes mellitus (T2DM). This trial was undertaken with the objective of evaluating the effect of adding different concentrations of magnesium chloride to the desalinated drinking water on the glycemic, metabolic, and insulin resistance parameters among patients with T2DM. A randomized cross-sectional controlled clinical trial was conducted to evaluate the effects of adding magnesium chloride supplement to desalinated drinking water consumed by patients with T2DM on the glycemic and metabolic parameters and indicators of insulin sensitivity. The total number of patients with T2DM who successfully completed the trial is 102. Patients were randomly allocated into three groups: the first group received bottled water without added magnesium (0 mg/L) (Group A, n = 37); the second group received bottled water with a low level of magnesium (20 mg/L) (Group B, n = 33); and the third group received drinking water with a high level of magnesium (50 mg/L) (Group C, n = 32). The daily consumption of elemental magnesium for a period of 3 months resulted in significant improvement in HbA1C (8.0 vs 8.2%, p = 0.04), insulin level (7.5 vs 9.9 μIU/mL, p = 0.03), and homeostasis model assessment-estimated insulin resistance (HOMA.IR) (2.5 vs 2.9, p = 0.002) in group C. However, there was no significant improvement in fasting blood glucose (FBS) level or lipid profile. The results of this study suggest that oral magnesium supplementation at the given dose of 50 mg/L daily added to drinking water could improve long-term glycemic control indicators and reduce insulin resistance in patients with T2DM.

Effect of oral magnesium supplement on cardiometabolic markers in people with prediabetes: a double blind randomized controlled clinical trial

To evaluate the effect of magnesium supplementation on insulin resistance and cardiovascular markers in people with prediabetes. A 12 week double-blind placebo-controlled randomized clinical trial was conducted at Isfahan Endocrine and Metabolism Research Center, Iran, on people with prediabetes (n = 86) to compare the effects of magnesium oxide 250 mg/day versus a placebo on anthropometric indices, blood pressure, fasting glucose, insulin, HOMA-IR index, C-reactive protein, uric acid and lipid profile. Both groups had similar distributions of anthropometric and biochemical variables at baseline. Those who received magnesium supplementation had significantly higher levels of HDL-cholesterol compared to the placebo group at the end of the study (49.7 ± 10.9 vs 43.6 ± 7.2 mg/dL, P = 0.003). The mean changes of HOMA-IR index, total cholesterol, LDL-cholesterol, triglyceride, uric acid and C-reactive protein levels as well as anthropometric indices and blood pressure in supplemented and placebo groups did not differ significantly. Magnesium supplementation increased HDL-cholesterol levels in people with prediabetes. However, other cardiometabolic markers were not improved by magnesium supplementation at the above dosage and duration.

Reduced serum magnesium is associated with the occurrence of diabetic macular edema in patients with diabetic retinopathy: A retrospective study.

Serum magnesium levels have been reported to reflect the risk of diabetic retinopathy (DR); however, the effect of serum magnesium level on diabetic macular edema (DME) remains unclear. Here, we investigated the association between the serum magnesium levels and DME in patients with DR. Patients with DR were recruited between January 2018 and June 2021. A total of 519 such patients were included in this study. All patients underwent a standardized clinical ophthalmic examination by an experienced ophthalmologist, and an assay was conducted to determine the serum magnesium concentration. Compared with the non-DME group, the DME group had a higher proportion of insulin use and a higher level of serum ischemia-modified albumin and fasting plasma glucose. The serum magnesium and calcium levels were lower in the DME group than in the non-DME group (P < 0.05). Higher magnesium levels were negatively associated with DME after adjustment for relevant covariates. Compared with the participants in the lowest magnesium quartile, those in the fourth quartile showed a significantly lower risk of DME after adjustment [odds ratio (OR), 0.294; 95% confidence interval, 0.153–0.566; P < 0.0001]. Considering the potentially different effects of serum magnesium on the development of DME in patients with DR based on age, DR staging and insulin use, stratified analysis was performed by considering these factors. Among insulin-using patients with non-proliferative DR who were < 66 years of age, those in the third and fourth quartile of serum magnesium were less likely to develop DME than those in the lowest quartile of serum magnesium [OR (95% CI), 0.095 (0.014–0.620), 0.057 (0.011–0.305); P = 0.014, 0.001]. Overall, a higher serum magnesium level was associated with a lower risk of DME in patients with DR. Furthermore, patients with DR who used insulin were more likely to develop DME. Long-term studies on oral magnesium supplements are needed to determine whether maintaining the serum magnesium levels in a higher physiological range can reduce the risk of DME in patients with DR.

Reversal Of Arterial Disease by modulating Magnesium and Phosphate (ROADMAP-study): rationale and design of a randomized controlled trial assessing the effects of magnesium citrate supplementation and phosphate-binding therapy on arterial stiffness in moderate chronic kidney disease

BackgroundArterial stiffness and calcification propensity are associated with high cardiovascular risk and increased mortality in chronic kidney disease (CKD). Both magnesium and phosphate are recognized as modulators of vascular calcification and chronic inflammation, both features of CKD that contribute to arterial stiffness. In this paper, we outline the rationale and design of a randomized controlled trial (RCT) investigating whether 24 weeks of oral magnesium supplementation with or without additional phosphate-binding therapy can improve arterial stiffness and calcification propensity in patients with stage 3–4 CKD.MethodsIn this multi-center, placebo-controlled RCT, a total of 180 participants with an estimated glomerular filtration rate of 15 to 50 ml/min/1.73 m2 without phosphate binder therapy will be recruited. During the 24 weeks intervention, participants will be randomized to one of four intervention groups to receive either magnesium citrate (350 mg elemental magnesium/day) or placebo, with or without the addition of the phosphate binder sucroferric oxyhydroxide (1000 mg/day). Primary outcome of the study is the change of arterial stiffness measured by the carotid-femoral pulse wave velocity over 24 weeks. Secondary outcomes include markers of calcification and inflammation, among others calcification propensity (T50) and high-sensitivity C-reactive protein. As explorative endpoints, repeated 18F-FDG and 18F-NaF PET-scans will be performed in a subset of participants (n = 40). Measurements of primary and secondary endpoints are performed at baseline, 12 and 24 weeks.DiscussionThe combined intervention of magnesium citrate supplementation and phosphate-lowering therapy with sucroferric oxyhydroxide, in stage 3–4 CKD patients without overt hyperphosphatemia, aims to modulate the complex and deregulated mineral metabolism leading to vascular calcification and arterial stiffness and to establish to what extent this is mediated by T50 changes. The results of this combined intervention may contribute to future early interventions for CKD patients to reduce the risk of CVD and mortality.Trial registrationNetherlands Trial Register, NL8252 (registered December 2019), EU clinical Trial Register 2019-001306-23 (registered November 2019).

Comparison of Oral Magnesium Supplements with Placebo for Pregnancy-Induced Leg Cramps

Background: Magnesium deficiency results in different types of complications in the pregnant females in pre and post delivery phase. This study is planned to check the impact of magnesium supplementation in terms of reduced leg cramps. Objective: To compare the effectiveness of oral magnesium supplements versus placebo for pregnancy-induced leg cramps. Study Design: Randomized control trial Place and Duration of Study: Department of Obstetrics &amp; Gynecology Department Unit 1, Lady Willingdon Hospital Lahore from 25th March 2017 to 30th September 2017. Methodology: Two hundred pregnant women were enrolled. All patients were divided in two groups and each group comprised 100 patients. Group A received magnesium bisglycinate chelate (300 mg per day) and group B received placebo. All patients of both groups were followed for effectiveness. At the end of the 4th week, a detailed history was taken from patients about entirely free from leg cramps i.e. effectiveness. Results: The mean age was 28.29±5.76 years. Gestational age was 27.74±5.25 weeks. The body mass index was &gt;30 in 141 (70%). Majority of the females 57 (28.5%) have parity 3 while 55 (27.5%) were having parity 2. Overall efficacy was 71 (35.5%) and it was not noted in 129 (64.5%). It was found that efficacy of magnesium was in 45 (45%) and in placebo group 26 (26%) and this difference was statistically significant (p&lt;0.05). Conclusion: Magnesium therapy appears to be effective in the treatment of pregnant induced leg cramps in the general population, but may have a small effect in pregnant women. Key Word: Leg cramps, Pregnancy, Magnesium therapy

P385 SYNCOPAL VENTRICULAR TACHYCARDIA IN HEALTHY HEART: AN UNUSUAL ORIGIN!

Abstract Torsade de pointes is a particular type of ventricular tachycardia, characterized by QRS complexes that vary progressively in amplitude and morphology, giving the impression of oscillating around the isoelectric line. Causes include long QT syndrome (congenital or drug–induced) or severe hypomagnesemia. We report the case of a 57–year–old woman, a smoker, with a history of weight loss in the last 6 months, hospitalized in Medicine for marked asthenia and an episode of fleeting loss of consciousness, from sitting. She was asymptomatic for chest pain. The physical examination showed a pathological thinness, with BMI 15 kg/m2, rhythmic cardiac activity, no murmurs, no signs of decompensation, flat abdomen, not enlarged liver. Pale, dry skin was observed. On ECG: sinus rhythm, HR 70 bpm, QTc slightly increased 0.47 sec, flat T wave in lateral. Blood exams evidenced: hypokalemia, hypomagnesemia, rise of the amylase. On the MRI abdomen we found large inhomogeneous areas on the head and body of the pancreas, referable to the picture of focal pancreatitis. For syncopal episode during hospitalization in Medicine, she was transferred in Cardiology, where, during electrocardiographic monitoring, paroxysmal ventricular tachycardias torsade de pointes–like, symptomatic, self–resolved was registered. We diagnosed an acute pancreatitis with typical radiological characteristics of an autoimmune form, determining severe electrolyte imbalance and consequent symptomatic paroxysmal ventricular tachycardias. Oral magnesium supplement and corticosteroid therapy allowed the resolution of the arrhythmic problem, monitored over time through the implantation of a loop recorder.

Bartter Syndrome in A Nigerian Child with Recurrent Vomiting

Bartter syndrome is a rare renal tubular disease characterized by hypokalemic metabolic alkalosis and renal salt wasting. There is paucity of report of this condition from Africa. We report a case of a four–year–old Nigerian boy who presented with growth failure, recurrent episodes of vomiting, features of severe dehydration and normal blood pressure warranting in–hospital care on several occasions over a period of 16 months. This patient had hypokalemia, hypochloremia, hyponatraemia and hypercalciuria. He also had abdominal x-ray findings of a triangular-shaped calcific density in the right renal bed suggestive of right medullary nephrocalcinosis. Diagnosis of Bartter syndrome was confirmed by elevated plasma renin of 8.1ng/ml/hr (normal 0.5 – 5.9). The patient was managed with intravenous normal saline, potassium chloride infusion, calcium gluconate, and then oral potassium, calcium and magnesium supplements. Follow up at the clinic revealed significant weight gain and stable clinical state. A high index of suspicion is needed for early diagnosis of this rare syndrome, particularly in children presenting with persistent vomiting, failure to thrive and dyselectrolytemia. This, invariably, will improve survival and health-related quality of life of such children, hence the need for this report.

MO1006: Cni-Induced Hypomagnesemia in Kidney Transplantation: A Comparative Monocentric Study Between Sucrosomial Magnesium and Magnesium Pidolate

Abstract BACKGROUND AND AIMS Magnesium (Mg) is the second cation in the intracellular space and the fourth prevalent cation in the body. It contributes to DNA and protein synthesis, infiammatory processes and cardiac excitability, while Mg deficiency leads to increased cardiovascular risk, atherosclerosis and diabetes [1]. In addition to gastrointestinal losses, loop or thiazide diuretics induce renal wasting, volume expansion and nephrotoxins including antibiotics Hypomagnesemia (HypoMg) is observed early after kidney transplantation and is associated with a faster decline of allograft function. Main determinants are calcineurin inhibitors (CNIs), protonic pump inhibitors (PPI), low Mg intake and diuretics. CNIs, in particular, induce HypoMg with mechanisms not fully understood, likely via downregulation of the Mg channel TRPM6 in the distal collecting tubule [2]. HypoMg should be corrected with oral supplements. Recently, in order to increase magnesium bioavailability and tolerance not shown by convetional oral magnesium supplements, a new sucrosomial magnesium formulation has been developed. Its innovative preparation encapsulates magnesium oxide in a phospholipid membrane covered by a sucrester matrix, which enhances Mg passage through the gastric and intestinal environment without any interaction with the intestinal mucosa [3]. This study evaluates magnesium bioavailability, tolerance and effectiveness after administration of sucrosomial magnesium compared with magnesium pidolate. METHOD We recruited 32 adult single, double or combined kidney-pancreas transplant recipients within 1 year from transplantation, who developed CNI-induced hypomagnesemia. Exclusion criteria include: HypoMg due to PPI or gastrointestinal losses. A total of 13 patients received magnesium pidolate, and 19 patients received sucrosomial magnesium. Venous blood samples were taken at baseline (T0) and after 10 days of magnesium supplement (T1). RESULTS Sucrosomial magnesium increased Mg bioavailability and tolerance: 0.60 ± 0.02 T0 mmoL/L versus 0.69 ± 0.05 T1; P &amp;lt; .0001 versus magnesium pidolate: 0.61 ± 0.05 T0 versus 0.64 ± 0.05 T1; P = .72 N.S. (Fig. 1A). Sucrosomial magnesium provided an increase of Mg over magnesium pidolate in terms of $\Delta \% $ increase: 12.4% for sucrosomial Mg versus 5.4%, P = .04 (Fig. 1B). CONCLUSION Our data, although obtained by a small cohort of transplant patients, shows that sucrosomial Mg is more efficient and better tolerated compared with magnesium pidolate. On the one hand, the fact that our study is the first in transplant patients to evaluate the impact of sucrosomial Mg for the correction of HypoMg might justify the limited number of patients enrolled and the short observation time; on the other hand, our results could serve as a working hypothesis for further studies with a larger number of transplant patients and for extended study duration to confirm the benefit of sucrosomial Mg.