Baseline Serum Magnesium Levels Research Articles

Hypomagnesemia as a predictor of the efficacy of combination EGFR-targeted drugs versus EGFR ADCs alone in HNSCC.

146 Background: EGFR-targeted drugs and ADCs in combination with EGFR-conjugated chemotherapy drugs can both cause hypomagnesemia. However, the predictive value of hypomagnesemia in response to treatment for head and neck squamous cell carcinoma (HNSCC) is unclear. Methods: This study retrospectively analyzed patients who participated in clinical trials of EGFR-targeted drugs and EGFR ADCs for HNSCC and solid tumors, from February 24, 2022, to March 25, 2024. The primary endpoint of the study was time to treatment failure (TTF). Results: This study conducted a retrospective analysis of 68 patients . All patients exhibited normal baseline serum magnesium levels prior to treatment, but following two cycles of treatment, varying degrees of hypomagnesemia were observed among them. Among the 46 patients who received 2 cycles of combination therapy with EGFR-targeted drugs, 33 were hypomagnesemia and 13 were normal serum magnesium, ORR[90.9%vs. 8.5%,(P=0.002)] (Table), TTF [151 days (95% CI: 212-380) vs. 87 days (95% CI: 52-230), HR 0.576 (95% CI: 0.270–1.230,P = 0.021)]. Among the 22 patients who received EGFR ADC alone for 2 cycles, 8 were hypomagnesemia and 14 were normal serum magnesium, ORR [37.5% vs.28.6%, (P=0.549)] (Table), TTF [97.5 days (95% CI: 68-300) vs. 108.5 days (95% CI: 60-160), HR of 0.877 (95% CI: 0.339–2.263; P = 0.547)]. Conclusions: The study demonstrates that, the occurrence of hypomagnesemia is associated with ORR and TTF following two cycles of combination of EFGR-targeted drugs, not observed in patients receiving EGFR ADCs as monotherapy in HNSCC. [Table: see text]

Association Between Serum Magnesium Levels and Outcomes of Atezolizumab in Patients With Metastatic Urothelial Carcinoma.

Evidence suggests that serum magnesium levels are associated with outcomes of immune checkpoint inhibitors (ICIs). However, this association remains under-explored in patients with metastatic urothelial carcinoma (UC) treated with ICIs. This prognostic study used individual participant-level data from 1,281 patients with locally advanced or metastatic UC treated with atezolizumab (N=855) or chemotherapy (N=426) who participated in the IMvigor210 and the IMvigor211 trials. Multivariable Cox proportional hazards regression and Fine-Gray subdistribution hazards regression models were used to examine the association of baseline serum magnesium levels with overall survival (OS), progression-free survival (PFS), and immune-related adverse events (irAEs). No evidence of an association was found between baseline serum magnesium levels and PFS or OS in patients treated with atezolizumab [PFS, hazard ratio (HR)=1.03, 95% confidence interval (CI)=0.78-1.35; OS, HR=1.13, 95%CI=0.84-1.51] or chemotherapy (PFS, HR=0.93, 95%CI=0.62-1.40; OS, HR=0.91, 95%CI=0.59-1.40). We also found no evidence of association with irAEs (subdistribution HR=1.29, 95%CI=0.81-2.07) in patients receiving atezolizumab. This study found no evidence of an association between baseline serum magnesium levels and treatment outcomes or irAEs in patients with metastatic UC receiving atezolizumab. Contrary to previous research suggesting a role for magnesium in cancer therapy, these results indicate that serum magnesium levels may not serve as a biomarker to predict outcomes in these patients.

Serum Magnesium Levels and Cardiovascular Outcomes in Systolic Blood Pressure Intervention Trial Participants

Serum magnesium levels have been inversely yet inconsistently associated with cardiovascular (CV) outcomes. In this study, we examined the association of serum magnesium levels with CV outcomes in the Systolic Blood Pressure Intervention Trial (SPRINT) participants. Case-control post hoc analysis of SPRINT. A total of 2,040 SPRINT participants with available serum samples at baseline level were included in this study. Case participants (n=510) who experienced a CV event during the SPRINT observation period (median follow-up of 3.2 years) and control participants (n=1,530) without CV events were sampled in a 1:3 ratio for measurements of serum magnesium level at baseline and 2-year follow-up. Baseline serum magnesium levels and 2-year percentage change in serum magnesium levels (ΔSMg). SPRINT primary composite CV outcome. Multivariable conditional logistic regression analysis, accounting for matching factors, was used to evaluate the association of baseline and ΔSMg with CV outcomes. Individual matching of cases and controls was based on the SPRINT treatment arm allocation (standard vs intensive) and prevalence of chronic kidney disease (CKD). The median serum magnesium level at baseline was similar among the case and control groups. In a fully adjusted model, each standard deviation (SD) (0.18mg/dL) higher of the baseline serum magnesium level was independently associated with a lower risk for composite CV outcomes in all study participants (adjusted odds ratio 95% CI, 0.79 [0.70-0.89]). This association was similar when serum magnesium levels were analyzed in quartiles but dissipated in the standard (vs intensive) arm of SPRINT (0.88 [0.76-1.02] vs 0.65 [0.53-0.79], respectively; Pinteraction=0.06). The presence or absence of CKD at baseline did not modify this association. ΔSMg was not independently associated with CV outcomes occurring after 2 years. ΔSMg was small in magnitude, limiting effect size. Higher baseline serum magnesium levels were independently associated with reduced risk for CV outcomes in all study participants, but ΔSMg was not associated with CV outcomes.

Low Serum Magnesium Levels Are Associated With Hemorrhagic Transformation After Mechanical Thrombectomy in Patients With Acute Ischemic Stroke

ObjectiveIn patients with acute ischemic stroke (AIS), hemorrhagic transformation (HT) is a major complication after mechanical thrombectomy (MT). This study aimed to investigate the relationship between serum magnesium levels and HT after MT.MethodsWe collected 199 cases of consecutive AIS that received MT due to acute anterior circulation occlusions in our institution between January 2017 and January 2020. Baseline serum magnesium was obtained from all patients on admission before MT. The patients were divided into two groups based on the occurrence of HT. Univariate and multivariate analyses were performed to investigate whether magnesium was an independent predictor of HT. The receiver operating characteristic (ROC) curve and area under the curve (AUC) were determined.ResultsOf the 199 enrolled patients, 40 (20.1%) presented with HT, and 12 (6%) developed symptomatic intracranial hemorrhage (sICH). Patients with HT had lower serum magnesium levels compared to those without HT (0.76 [0.69–0.80] vs. 0.84 [0.80–0.90], p < 0.001). The multivariate logistic analysis showed that the serum magnesium level (odds ratio, [OR]: 0.000, 95% confidence interval [CI]: 0.000–0.001, p < 0.001) was significantly associated with the occurrence of HT. The ROC curve analysis revealed that the serum magnesium level could predict HT with an AUC of.820 (95% CI: 0.750–0.891 p < 0.001). Serum magnesium ≤ 0.80 mmol/L could predict HT with a sensitivity of 79.2% and a specificity of 70.0%. Of interest, the serum magnesium level was not associated with HT when the baseline of serum magnesium was higher than the cut-off value (0.80 mmol/L) in the subgroup analysis.ConclusionsLower baseline serum magnesium levels (<0.80 mmol/L) on admission are associated with increased risk of HT in AIS patients receiving MT.

Rapid Treatment with Intramuscular Magnesium Sulfate During Cardiopulmonary Resuscitation Does Not Provide Neuroprotection Following Cardiac Arrest.

Brain injury is the most common cause of death for patients resuscitated from cardiac arrest. Magnesium is an attractive neuroprotective compound which protects neurons from ischemic injury by reducing neuronal calcium overload via NMDA receptor modulation and preventing calcium-induced mitochondrial permeability transition. Intramuscular (IM) delivery of MgSO4 during CPR has the potential to target these mechanisms within an early therapeutic window. We hypothesize that IM MgSO4 administrated during CPR could achieve therapeutic serum magnesium levels within 15min after ROSC and improve neurologic outcomes in a rat model of asphyxial cardiac arrest. Male Long Evans rats were subjected to 8-min asphyxial cardiac arrest and block randomized to receive placebo, 107mg/kg, 215mg/kg, or 430mg/kg MgSO4 IM at the onset of CPR. Serum magnesium concentrations increased rapidly with IM delivery during CPR, achieving twofold to fourfold increase by 15min after ROSC in all magnesium dose groups. Rats subjected to cardiac arrest or sham surgery were block randomized to treatment groups for assessment of neurological outcomes. We found that IM MgSO4 during CPR had no effect on ROSC rate (p > 0.05). IM MgSO4 treatment had no statistically significant effect on 10-day survival with good neurologic function or hippocampal CA1 pyramidal neuron survival compared to placebo treatment. In conclusion, a single dose IM MgSO4 during CPR achieves up to fourfold baseline serum magnesium levels within 15min after ROSC; however, this treatment strategy did not improve survival, recovery of neurologic function, or neuron survival. Future studies with repeated dosing or in combination with hypothermic targeted temperature management may be indicated.

Case Report and Supporting Documentation: Acute Kidney Injury Manifested as Oliguria Is Reduced by Intravenous Magnesium Before Cisplatin

After more than four decades of post-approval, cisplatin is still an important treatment for numerous cancers. However, acute kidney injury (AKI), defined as significant impairment of renal filtration as discussed below, is the major limiting side effect of cisplatin, occurring in approximately 30% of patients (25–33% after the first course). Cisplatin also damages the kidneys’ ability to reabsorb magnesium in 40–100% of patients, with collateral health risks due to subsequent hypomagnesemia. Multiple methods and drugs have been proposed for preventing cisplatin-induced AKI, including saline infusion with or without mannitol, which has not always prevented AKI and has been found to activate a cellular stress response in renal tubular cells. While numerous reports and trials, as well as the National Comprehensive Cancer Network (NCCN), support premedication with magnesium and hydration, this practice has not been universally accepted. Many clinics administer intravenous magnesium (IV) only after identification of hypomagnesemia post-cisplatin treatment, thus placing patients at risk for AKI and chronic renal loss of magnesium. We present the following case report and additional supporting evidence identifying the immediate effect of IV magnesium prior to intraperitoneal cisplatin for cycle 4 because of documented hypomagnesemia resulting in normalization of oliguria, which had been experienced for the first three cycles. The patient subsequently requested and received IV magnesium before cisplatin for the next two cycles with continuation of normal urinary output. The effect of pretreatment with IV magnesium on urine output following cisplatin has not been previously reported and further supports pre-cisplatin administration. In addition, two recent meta-analyses of clinical trials and pre-clinical research are reviewed that demonstrate effectiveness of magnesium pretreatment to preventing AKI without reducing its chemotherapeutic efficacy. This case report with additional evidence supports the adoption of administration of 1–3 g IV magnesium before cisplatin as best practice to prevent cisplatin induced AKI and hypomagnesemia regardless of patient baseline serum magnesium levels.

Low Serum Magnesium Levels Are Associated With Hemorrhagic Transformation After Thrombolysis in Acute Ischemic Stroke.

Background: In patients with acute ischemic stroke, hemorrhagic transformation is a major complication after intravenous thrombolysis. This study aimed to investigate the relationship between serum magnesium levels and hemorrhagic transformation (HT) after thrombolytic therapy.Methods: We retrospectively analyzed data from 242 patients who received thrombolytic therapy at the Second Affiliated Hospital of the Wenzhou Medical University in China. Baseline serum magnesium levels were measured before intravenous thrombolysis, and the occurrence of HT was evaluated using computed tomography images reviewed within 24–36 h after therapy. The relationship between serum magnesium levels and HT was examined using multivariate logistic regression, subgroup analysis, and restricted cubic spline models.Results: Of the 242 included patients, 43 (17.8%) developed HT. Patients with HT had significant lower serum magnesium levels than those without HT (0.81 ± 0.08 vs. 0.85 ± 0.08 mmol/L, p = 0.007). Multivariable logistic regression analysis indicated that patients with higher serum magnesium levels had lower risk of HT (OR per 0.1-mmol/L increase 0.43, 95% CI 0.27–0.73, p = 0.002). However, this association did not persist when baseline levels of serum magnesium were higher than the median value (0.85 mmol/L) in subgroup analysis (OR per 0.1-mmol/L increase 0.58, 95% CI 0.14–2.51, p = 0.47). This threshold effect was also observed in the restricted cubic spline model when serum magnesium levels were above 0.88 mmol/L. No association between symptomatic HT and serum magnesium levels was observed in our study (OR per 0.1-mmol/L increase 0.52, 95% CI 0.25–1.11, p = 0.092).Conclusions: Lower serum magnesium levels in patients with ischemic stroke are associated with an increased risk of HT after intravenous thrombolysis, but perhaps only when serum magnesium is below a certain minimal concentration.

Proton pump inhibitor as an independent factor of progression of abdominal aortic calcification in patients on maintenance hemodialysis.

BackgroundsProton pump inhibitors (PPIs) can be associated with vascular calcification in patients undergoing dialysis through hypomagnesemia. However, only few studies have demonstrated the influence of PPIs on vascular calcification in patients on maintenance hemodialysis (HD). This study aimed to investigate whether the use of PPIs accelerates vascular calcification in patients on HD.Materials and methodsWe retrospectively evaluated 200 HD patients who underwent regular blood tests and computed tomography (CT) between 2016 and 2017. The abdominal aortic calcification index (ACI) was measured using abdominal CT. The difference in the ACI values between 2016 and 2017 was evaluated as ΔACI. Patients were divided into PPI and non-PPI groups, and variables, such as patient background, medication, laboratory data, and ΔACI were compared. Factors independently associated with higher ΔACI progression (≥ third tertile value of ΔACI in this study) were determined using multivariate logistic regression analysis.ResultsThe PPI and non-PPI groups had 112 (56%) and 88 (44%) patients, respectively. Median and third tertile value of ΔACIs were 4.2% and 5.8%, respectively. Serum magnesium was significantly lower in the PPI (2.1 mg/dL) than in the non-PPI (2.3 mg/dL) group (P <0.001). Median ΔACI was significantly higher in the PPI (5.0%) than in the non-PPI (3.8%) group (P = 0.009). A total of 77 (39%) patients had a higher ΔACI. Multivariate analysis revealed that PPIs (odds ratio = 2.23; 95% confidence interval = 1.11–4.49), annual mean calcium phosphorus product, ACI in 2016, baseline serum magnesium levels, and HD vintage were independent factors associated with higher ΔACI progression after adjusting for confounders.ConclusionPPI use may accelerate vascular calcification in patients on HD. Further studies are necessary to elucidate their influence on vascular calcification.

Short-Term Effect of High-Dose Pantoprazol on Serum and Urinary Magnesium Levels.

Proton pump inhibitor (PPI) induced hypomagnesemia is a completely unexplained issue and cases are still being reported. Long-term use is the main factor, but there are a few articles stating that it may also emerge with short-term use. We aimed to evaluate the changes of serum and urine magnesium levels during shortterm high dose pantoprazol treatment. The serum and 24-hour urine magnesium levels of 58 patients were evaluated during the course of 2 days. Of 58 patients, 25 were allowed oral intake on the 3rd day of hospitalization and thus, 24-hour urine for 3 days was collected from 33 patients. There were no significant differences in the mean levels of serum magnesium and the median levels of urine magnesium. When the magnesium levels were evaluated by age over and under 60 years, the baseline serum magnesium level was significantly higher than the 1st level in patients aged ≥ 60 years (p = 0.029). The 3rd day serum magnesium level was significantly higher than the baseline and 1st day levels in those aged < 60 years (p = 0.049). We showed that plasma levels and urinary excretion of magnesium did not change significantly during high-dose pantoprazol treatment. It can be hypothesized that magnesium levels are not affected by PPIs in short-term usage. Age and other contributing factors may have more impact on PPI induced hypomagnesemia. Patients aged over 60 years might be handled carefully under proton pump inhibitors treatment.

Serum Magnesium Levels and Hospitalization and Mortality in Incident Peritoneal Dialysis Patients: A Cohort Study.

Prior studies have shown the association of low serum magnesium levels with adverse health outcomes in patients undergoing hemodialysis. There is a paucity of such studies in patients undergoing peritoneal dialysis (PD). Cohort study. 10,692 patients treated with PD from January 1, 2007, through December 31, 2011, in facilities operated by a single large dialysis organization in the United States. Baseline serum magnesium levels, examined as 5 categories (<1.8, 1.8-<2.0, 2.0-<2.2 [reference], 2.2-<2.4, and≥2.4mg/dL). Time to first hospitalization and time to death using competing-risks regression models. The distribution of baseline serum magnesium levels in the cohort was<1.8mg/dL, 1,928 (18%); 1.8 to<2.0mg/dL, 2,204 (21%); 2.0 to<2.2mg/dL, 2,765 (26%); 2.2 to<2.4mg/dL, 1,765 (16%); and≥2.4mg/dL, 2,030 (19%). Of 10,692 patients, 6,465 (60%) were hospitalized at least once and 1,392 (13%) died during follow-up (median, 13; IQR, 7-23 months). Baseline serum magnesium level< 1.8mg/dL was associated with higher risk for hospitalization and all-cause mortality after adjustment for demographic and clinical characteristics (adjusted HRs of 1.23 [95% CI, 1.14-1.33] and 1.21 [95% CI, 1.03-1.42], respectively). The higher risk for hospitalization persisted upon adjustment for laboratory variables, whereas that for all-cause mortality was attenuated to a nonsignificant level. The greatest risk for hospitalization was in patients with low serum albumin levels (<3.5g/dL; P for interaction< 0.001). Possibility of residual confounding by unmeasured variables cannot be excluded. Lower serum magnesium levels may be associated with higher risk for hospitalization in incident PD patients, particularly those with hypoalbuminemia. Additional studies are needed to confirm these findings and investigate whether correction of hypomagnesemia reduces these risks.

Association of Serum Magnesium Level with Odds of Prediabetes and Diabetes in a Southern Chinese Population: a Prospective Nested Case-Control Study.

Although emerging clinical evidence supports that magnesium deficiency is a risk factor for the development of type 2 diabetes, there are sparse studies concerning the dynamic change of serum magnesium with the risk of diabetes and its early stages. In this nested case-control study, we performed a 75-g oral glucose tolerance test or a standardized steamed bread meal test in 178 subjects with incident glucose metabolism impairment (33 with type 2 diabetes and 145 with prediabetes) and 178 matched controls at baseline and at 3-year follow-up and determined the associations between baseline serum magnesium levels as well as changes in serum magnesium levels at follow-up and odds of prediabetes and diabetes. After adjusting for potential confounders, the odds ratios of risk for prediabetes and type 2 diabetes in the highest quartile of serum magnesium levels were 0.22 (95% confidence intervals [CI] 0.10-0.49; p for trend <0.001) and 0.02 (95% CI 0.00-0.29; p for trend = 0.009), respectively, as compared with the lowest quartile. In addition, a significant decline in the serum magnesium level was detected in type 2 diabetes cases (p = 0.015) at 3years as compared with at baseline. These results suggest that a low magnesium level is an independent risk factor for prediabetes and type 2 diabetes, and that the reduction of serum magnesium is associated with type 2 diabetes in a southern Chinese population.

Hypomagnesemia and the Risk of New-Onset Diabetes Mellitus after Kidney Transplantation

Several studies suggest a link between post-transplant hypomagnesemia and new-onset diabetes after transplantation (NODAT), but this relationship remains controversial. We conducted a retrospective cohort study of 948 nondiabetic kidney transplant recipients from January 1, 2000, to December 31, 2011, to examine the association between serum magnesium level and NODAT. Multivariable Cox proportional hazards models were fitted to evaluate the risk of NODAT as a function of baseline (at 1 month), time-varying (every 3 months), and rolling-average (i.e., mean for 3 months moving at 3-month intervals) serum magnesium levels while adjusting for potential confounders. A total of 182 NODAT events were observed over 2951.2 person-years of follow-up. Multivariable models showed an inverse relationship between baseline serum magnesium level and NODAT (hazard ratio [HR], 1.24 per 0.1 mmol/L decrease; 95% confidence interval [95% CI], 1.05 to 1.46; P=0.01). The association with the risk of NODAT persisted in conventional time-varying (HR, 1.32; 95% CI, 1.14 to 1.52; P<0.001) and rolling-average models (HR, 1.34; 95% CI, 1.13 to 1.57; P=0.001). Hypomagnesemia (serum magnesium <0.74 mmol/L) also significantly associated with increased risk of NODAT in baseline (HR, 1.58; 95% CI, 1.07 to 2.34; P=0.02), time-varying (HR, 1.78; 95% CI, 1.29 to 2.45; P<0.001), and rolling-average models (HR, 1.83; 95% CI, 1.30 to 2.57; P=0.001). Our results suggest that lower post-transplant serum magnesium level is an independent risk factor for NODAT in kidney transplant recipients. Interventions targeting serum magnesium to reduce the risk of NODAT should be evaluated.

Hypomagnesemia is a significant predictor of cardiovascular and non-cardiovascular mortality in patients undergoing hemodialysis

Although previous studies in the general population showed that hypomagnesemia is a risk for cardiovascular diseases (CVD), the impact of magnesium on the prognosis of patients on hemodialysis has been poorly investigated. To gain information on this we conducted a nationwide registry-based cohort study of 142,555 hemodialysis patients to determine whether hypomagnesemia is an independent risk for increased mortality in this population. Study outcomes were 1-year all-cause and cause-specific mortality with baseline serum magnesium levels categorized into sextiles. During follow-up, a total of 11,454 deaths occurred, of which 4774 had a CVD cause. In a fully adjusted model, there was a J-shaped association between serum magnesium and the odds ratio of all-cause mortality from the lowest to highest sextile, with significantly higher mortality in sextiles 1-3 and 6. Similar associations were found between magnesium and both CVD and non-CVD mortality. The proportion of patients with a baseline intact parathyroid hormone level under 50 pg/ml was significantly higher in the highest sextile; however, after excluding these patients, the CVD mortality risk in the highest sextile was attenuated. Thus, hypomagnesemia was significantly associated with an increased risk of mortality in hemodialysis patients. Interventional studies are needed to clarify whether magnesium supplementation is beneficial for improving patient prognosis.

The effect of intravenous magnesium therapy on the duration of intrathecal fentanyl labor analgesia

BackgroundMagnesium has been reported to augment the analgesic effects of opioids when co-administered into the cerebrospinal fluid. The purpose of this study was to determine the influence of intravenous magnesium therapy administered for preeclampsia on the duration of intrathecal fentanyl analgesia for labor. MethodsThirty-four nulliparous parturients having labor induced for preeclampsia and receiving intravenous magnesium therapy were recruited. Thirty-four nulliparous patients having labor induced for elective or medical reasons were recruited as controls. At request for analgesia, baseline serum magnesium levels were obtained and combined spinal–epidural analgesia was initiated with intrathecal fentanyl 25μg. Before injection of fentanyl, a sample of cerebrospinal fluid was obtained for magnesium assay. An epidural catheter was sited but no additional medications were administered until the second request for analgesia. The primary outcome was duration of intrathecal fentanyl analgesia. ResultsThere was no difference in the median duration of analgesia between the magnesium [79min (95% CI 76 to 82)] and control groups [69min (95% CI 56 to 82)] (difference between medians: 10min (95% CI −4 to 21min; P=0.16). There was neither a relationship between the serum and cerebrospinal fluid magnesium concentrations nor the cerebrospinal magnesium concentration and duration of intrathecal fentanyl analgesia. ConclusionsIntravenous magnesium therapy at doses typically used for seizure prophylaxis in preeclampsia did not influence the duration of intrathecal fentanyl labor analgesia. However, this study may have been underpowered to detect a difference and future study is warranted.

Intravenous magnesium sulfate enhances the ability of dofetilide to successfully cardiovert atrial fibrillation or flutter: results of the Dofetilide and Intravenous Magnesium Evaluation

A previous study found that the adjunctive use of intravenous magnesium sulfate with ibutilide could increase the odds of a patient chemically cardioverting from atrial fibrillation (AF) or flutter (AFL) to normal sinus rhythm (NSR) by 78%. Whether or not intravenous magnesium has the same effect on dofetilide's ability to chemically cardiovert patients from AF/AFL to NSR is not known. This was a retrospective cohort evaluation of consecutive eligible patients receiving dofetilide for chemical cardioversion of AF or AFL at a single institution. All AF or AFL patients received dofetilide according to the institution's standard protocol, which required patients to remain as an inpatient for a minimum of 3 days or 6 doses after the initiation of dofetilide therapy. Patients receiving any dose of intravenous magnesium starting on the same day as dofetilide constituted the treatment group. Controls received dofetilide, but no intravenous magnesium any time prior to chemical cardioversion. Patients underwent continuous electrocardiographic monitoring throughout their hospital admission. Multivariable logistic regression analysis was used to determine the impact of intravenous magnesium on dofetilide's efficacy. A total of 160 patients in persistent AF or AFL (mean age 66.6 +/- 11.0 years, 70.0% male, 30.0% in AF or AFL >15 days, 54.4% hypertension, 37.5% heart failure, 16.3% valvular disease, 16.3% previous myocardial infarction, and baseline serum magnesium levels 2.1 +/- 0.26 mg/dL) and receiving dofetilide (mean dose 428 +/- 118 microg/dose) were included in this analysis. The overall chemical cardioversion rate with dofetilide irrespective of adjunctive intravenous magnesium utilization was 41.9%. The concurrent administration of intravenous magnesium (n = 50) was associated with a 107% increased odds of successful chemical cardioversion [adjusted odds ratio: 2.07 (95% confidence intervals: 1.00-4.33)] compared with those who did not receive magnesium (n = 110). Only one case of torsade de pointes occurred in the no magnesium group during the index hospital admission. Concurrent use of intravenous magnesium is associated with an enhanced ability of dofetilide to successfully convert AF or AFL.

Magnesium utilization survey in selected patients with diabetes

Patients with diabetes mellitus were surveyed to determine magnesium utilization and supplementation patterns and the extent to which these patterns correlate with American Diabetes Association (ADA) consensus panel recommendations. Participating ADA member physicians were asked to enroll five or more patients with insulin-dependent diabetes mellitus (IDDM, or type I diabetes) or non—insulin-dependent diabetes mellitus (NIDDM, or type II diabetes) who were not currently receiving magnesium supplementation and who they believed required or could benefit from oral magnesium chloride administration. Data were then collected regarding specific patient characteristics (ie, current diabetes therapy and glucose control); concomitant diseases and cardiovascular medications; baseline serum magnesium level, if measured before initiating magnesium chloride supplementation; and magnesium chloride dosage and duration. A total of 199 patients with diabetes began treatment with magnesium chloride supplementation after enrollment by a specialist. The mean baseline serum magnesium level for patients with IDDM was 1.48 mg/dL and for patients with NIDDM was 1.4 mg/dL (normal range, 1.80 to 2.40 mg/dL). No differences in mean serum magnesium levels were observed between men and women and between those with IDDM and those with NIDDM. Glucose control, as measured by glycosylated hemoglobin A 1c, did not correlate with magnesium serum levels. A concomitant cardiovascular disease was present in 70% of patients. In 78.3% of patients, supplementation was initiated because of low serum magnesium levels; in 21.7%, magnesium chloride therapy was initiated empirically. No correlation was found between serum magnesium levels and the prescribed dosage or the recommended duration of magnesium therapy. Patterns of magnesium utilization among survey respondents generally followed ADA consensus panel recommendations. A majority of diabetic patients who were given magnesium chloride supplementation had concomitant cardiovascular disease. Primary care physicians and cardiologists who treat large numbers of patients with diabetes and cardiovascular disease should be knowledgeable of the ADA consensus report because of the high prevalence of hypomagnesemia and because of the consequences of magnesium deficiency in these high-risk groups. To achieve successful long-term maintenance in these patients, additional physician education appears to be necessary regarding initial dosing strategies and recommended duration of supplementation.