Mean Serum Magnesium Levels Research Articles

Serum magnesium in diabetic retinopathy: relation to glycated haemoglobin and lipid profile

The aim of this study was to evaluate serum magnesium status in diabetic retinopathy and to investigate its relation to serum lipid profile and glycated haemoglobin (HbA1c) as a marker for long- term metabolic control in diabetes. The current case control study has enrolled 25 type 2 diabetics without retinopathy (Group 1), 25 diabetics with retinopathy (Group 2) and 21 apparently healthy non- diabetic control subjects (Group 3). Overnight fasting serum magnesium, lipid profile and HbA1c concentration were analyzed for all subjects. The mean serum magnesium level was significantly lower in Group (2) compared to that of Group 1 (p< 0.001). The mean serum triglycerides (TGs) and HbA1c levels were significantly higher in Group 2 (p< 0.0001). No statistically significant differences were noticed comparing the mean serum total cholesterol (TC) and LDL-cholesterol concentrations in both groups 1 and 2 (p> 0.05). The study revealed a significant negative correlation between serum magnesium on one hand and serum TGs, TC, LDL- cholesterol and HbA1c on the other hand where r= - 0.646, - 0.47, - 0.335, and - 0.825 respectively. Meanwhile serum magnesium was significantly and positively correlated with HDL- cholesterol levels (r= 0.395, p> 0.001). Using Forward Stepwise Multiple Regression analysis, the study revealed that hypomagnesaemia, poor glycaemic control and increasing duration of diabetes are the most important contributors to the cumulative risk for the development of diabetic retinopathy (Odds ratios 16.65, 566 and 7.36 respectively). In conclusion, magnesium depletion is a significant risk factor for, and a frequent finding in, diabetic retinopathy beside poor glycaemic control, dyslipidaemia (mainly hypertriglyceridaemia), and increasing duration of uncontrolled diabetes. The significant association between hypomagnesaemia and high fasting serum levels of TGs, TC, LDL-cholesterol and HbA1c would rather support the suggested role for magnesium depletion in the metabolic derangements associated with retinopathy in diabetic patients. Further studies on the effects of magnesium supplementation for diabetic patients are necessary to investigate the spectrum of metabolic improvements following magnesium therapy and the degree to which the risk of diabetic retinopathy might be reduced.

Hypomagnesaemia in cystic fibrosis patients referred for lung transplant assessment

Background Hypomagnesaemia in patients with cystic fibrosis (CF) is underrecognized although the true incidence is unknown. Many patients are asymptomatic, although severe deficiency may be associated with muscle weakness, cramps and tetany. Hypomagnesaemia may be a risk factor for post-transplant complications including convulsions, which may be exacerbated by the use of calcineurin inhibitors. The aims of the present study were to describe serum magnesium levels and to investigate the relationship between magnesium levels and age, and renal function measurements in patients with CF referred to a transplant centre for lung transplant assessment. Methods We reviewed the data of all 106 CF patients referred for transplant assessment from January 1995 to December 2003. Demographic and biochemical data were recorded and the explanatory variables were subjected to univariate analysis and linear regression analysis. Results Mean serum magnesium level was 0.75 mmol/L (range 0.46–1.03, normal range 0.74–1.1). 57% of patients had hypomagnesaemia. Serum magnesium levels were not associated with age, serum creatinine or GFR. Conclusions Hypomagnesaemia is a common finding in patients with CF referred for lung transplant assessment. Serum magnesium levels should be monitored in all CF patients being referred for lung transplant irrespective of the results of other renal function tests.

Serum Magnesium Levels in Normal and Pre-Eclamptic Gestation in Benin City

Introduction: Preeclampsia is a major cause of maternal and perinatal morbidity and mortality worldwide. There is at the moment no reliable marker for pre-eclampsia. Objective: To compare the serum magnesium levels in pre-eclamptic and normotensive pregnant women in Benin -City, Nigeria. Methods: A cross-sectional study of serum magnesium levels in normal and preeclamptic gestation in Nigerian women was conducted in a tertiary hospital. Results: Serum magnesium was determined in 65 pre-eclamptic and 65 normotensive pregnant women. The mean serum magnesium level in the normal pregnant women was 1.06 ± 0.33Mmol/Litre while in preeclampsia it was 0.69 ± 0.14 Mmol/l. The difference was statistically significant (P Keywords : Serum magnesium; pre-eclampsia maternal and perinatal morbidity and mortality. Nigerian Medical Journal Vol. 48 (1) 2007: pp. 21-23

Effects of gadopentetate dimeglumine and gadodiamide on serum calcium, magnesium, and creatinine measurements

To investigate the in vivo effects of gadodiamide (Gd-DTPA-BMA) and gadopentetate dimeglumine (Gd-DTPA) on the laboratory measurements of serum calcium, magnesium, and creatinine. Medical records from 1993 to 2004 were reviewed to identify inpatients for whom laboratory data were available regarding serum calcium, creatinine, and magnesium levels before and within one day after gadodiamide and gadopentetate dimeglumine enhanced MRI. Patients who underwent both gadolinium (Gd)-enhanced MRI and iodinated contrast-enhanced examinations on separate days within a six-month period were also identified to compare changes in serum creatinine. Serum creatinine did not increase in 2788 cases following gadopentetate dimeglumine and gadodiamide injection. By comparison, serum creatinine increased from 1.21 to 1.28 mg/dL following iodinated contrast, and there were 20 cases (2.6%) of contrast-induced nephrotoxicity (P < 0.01). Gadopentetate dimeglumine did not affect serum calcium or magnesium measurements. Following 1157 gadodiamide-enhanced examinations, measured serum calcium spuriously dropped from 8.65 to 8.33 mg/dL (P < 0.0001) and 34 patients had spurious critical hypocalcemia (<6 mg/dL). Of 60 patients with high-dose gadodiamide injection and renal insufficiency, 36.7% (N = 22) had spurious critical hypocalcemia immediately post MRI. In 216 patients with renal insufficiency, the mean serum magnesium level increased slightly from 1.69 to 1.77 mEq/L following gadodiamide injection (P < 0.0001). Gd-based contrast agents are safe for MRI and MR angiography (MRA), and do not induce nephrotoxicity. However, gadodiamide interferes with serum calcium and magnesium measurements-particularly at high doses and/or with renal insufficiency.

Increase in Serum Magnesium Level in Haemodialysis Patients Receiving Sevelamer Hydrochloride

Clinical studies have shown that sevelamer hydrochloride improves lipid profiles and attenuates the progression of the cardiovascular calcifications in haemodialysis patients. It is known that both of these properties are associated with increased magnesium levels. The effect of sevelamer on serum magnesium level is not well documented. The aim of this study was to determine the effects of sevelamer treatment on serum magnesium in haemodialysis patients and to assess the association of magnesium levels with lipid profiles and intact parathyroid hormone (iPTH). Phosphate binders were discontinued during a two week washout period. Forty-seven patients, whose serum phosphate was greater than 6.0 mg/dl at the end of washout, received sevelamer hydrochloride for eight weeks. The patients were then washed off sevelamer for another two weeks. Mean serum phosphorus concentration declined from 7.5 +/- 1.3 to 6.4 +/- 1.2 mg/dl (P < 0.001), mean serum magnesium levels increased from 2.75 +/- 0.35 to 2.90 +/- 0.41 mg/dl (P < 0.001) and median serum iPTH levels decreased from 297 to 213 pg/ml (P=0.001) during the eight weeks of sevelamer treatment. After the two week post-treatment washout phosphorus levels increased to 7.3 +/- 1.3 mg/dl (P < 0.001), magnesium levels were reduced to 2.77 +/- 0.39 mg/dl (P < 0.001) and iPTH levels increased to 240 pg/ml (P=0.012). No change was observed in serum calcium levels during the sevelamer treatment period and the subsequent washout period. The mean decline in total and low density lipoprotein (LDL) cholesterol during sevelamer treatment was 16.3 and 28.3 (P < 0.001), respectively. The mean increase in high density lipoprotein (HDL) cholesterol and in apolipoprotein A1 was 2.9 +/- 5.8 mg/dl (P=0.004) and 6.8 +/- 11.1 mg/dl (P=0.001), respectively. Multivariate analysis showed that the rise in serum magnesium concentration significantly correlated with reductions in iPTH levels (r=-0.40, P=0.016), but did not have any significant correlation with the changes in lipid profiles. Our findings indicate that patients on haemodialysis receiving sevelamer have a significant increase in serum magnesium concentrations. This increase in serum magnesium is associated with reduction in iPTH levels. The changes in lipid profiles of these patients however are not related to changes in serum magnesium levels.

Serum Magnesium Levels as Related to Symptomatic Vasospasm and Outcome Following Aneurysmal Subarachnoid Hemorrhage

Recent evidence suggests that magnesium may be neuroprotective in the setting of cerebral ischemia, and therapeutic magnesium infusion has been proposed for prophylaxis and treatment of delayed ischemic neurological deficit (DIND) resulting from vasospasm in patients with aneurysmal subarachnoid hemorrhage (SAH). We studied the association between serum magnesium levels, the development of DIND, and the outcomes of patients with SAH. We studied 128 consecutive patients with aneurysmal SAH treated at our institution between 1990 and 1997 who had a serum magnesium level measured at least once during the acute phase of their hospitalization. Delayed ischemic neurological deficit was defined as severe (major focal deficit or coma), moderate (incomplete focal deficit or decreased sensorium without coma), or none. There was no significant difference in mean, minimum, or maximum serum magnesium levels between patients with and without DIND (1.93, 1.83, 2.02 versus 1.91, 1.84, 1.97 mg/dL, respectively). Similarly, no difference was found in mean serum magnesium levels among patients with severe (1.94 mg/dL), moderate (1.92 mg/dL), or no DIND (1.91 mg/dL). Analyses of serum magnesium levels before (0-4 days following SAH), during (4-14 days following SAH), and after (greater than 14 days following SAH) the period of highest risk for vasospasm revealed no association with the development or severity of DIND. Permanent deficit or death resulting from vasospasm and Glasgow Outcome Scale score at longest follow-up were similarly unaffected by serum magnesium levels overall or during any time interval. Forty (31.5%) patients were hypomagnesemic (less than 1.7 mg/dL) during hospitalization, but no difference in outcome (p = 0.185) or development of DIND (p = 0.785) was found when compared to patients with normal (1.7-2.1 mg/dL) or high (greater than 2.1 mg/dL) magnesium serum levels. We identified no relationship between serum magnesium levels and the development of DIND or outcome following aneurysmal SAH. Based on these data, magnesium supplementation to normal or high-normal physiological ranges seems unlikely to be beneficial for DIND resulting from vasospasm. However, no inference can be made regarding the value of therapeutic infusion of magnesium to supraphysiological levels.

Low serum magnesium levels and metabolic syndrome.

Low serum magnesium levels are related to diabetes mellitus (DM) and high blood pressure (HBP), but as far as we know, there are no previous reports that analyzed the serum magnesium concentration in individuals with metabolic syndrome (MS). We performed a cross-sectional population-based study to compare 192 individuals with MS and 384 disorder-free control subjects, matched by age and gender. Magnesium supplementation treatment and conditions likely to provoke hypomagnesemia, including previous diagnosis of diabetes mellitus (DM) and/or high blood pressure (HBP), were exclusion criteria. In this regard, only incident cases of DM and HBP were included. MS was defined by the presence at least of two of the following features: hyperglycemia (> or =7.0 mmol/l); HBP (> or =160/90 mmHg); dyslipidemia (fasting triglycerides > or =1.7 mmol/l and/or HDL-cholesterol <1.0 mmol/l); and obesity (body mass index > or =30 kg/m(2) and/or waist-to-hip ratio > or =0.85 in women or > or =0.9 in men). Low serum magnesium levels were identified in 126 (65.6%) and 19 (4.9%) individuals with and without MS, p<0.00001. The mean serum magnesium level among subjects with MS was 1.8+/-0.3 mg/dl, and among control subjects 2.2+/-0.2 mg/dl, p<0.00001. There was a strong independent relationship between low serum magnesium levels and MS (odds ratio (OR)=6.8, CI(95%) 4.2-10.9). Among the components of MS, dyslipidemia (OR 2.8, CI(95%) 1.3-2.9) and HBP (OR 1.9, CI(95%) 1.4-2.8) were strongly related to low serum magnesium levels. This study reveals a strong relationship between decreased serum magnesium and MS.

Relationship between the serum parathyroid hormone and magnesium levels in continuous ambulatory peritoneal dialysis (CAPD) patients using low-magnesium peritoneal dialysate.

BackgroundPatients on continuous ambulatory peritoneal dialysis (CAPD) have increased risk of low-turnover bone disease and relative hypoparathyroidism. Recently, it has been believed that magnesium plays an important role in regulating secretion of parathyroid hormone (PTH). The aim of this study was to evaluate the relationship between serum PTH and serum magnesium as a factor increasing the frequency of relative hypoparathyroidism.MethodsWe analyzed the data of 56 patients who had been on CAPD for more than 6 months without any significant problems. No patient had been previously treated with vitamin D or aluminum hydroxide. The patients had used peritoneal dialysate with the magnesium concentration of 0.5 mEq/L. Biochemical parameters, such as BUN, creatinine, alkaline phosphatase bony isoenzyme, total protein, albumin, total calcium, ionized calcium and intact parathyroid hormone level were measured.ResultsThe mean serum magnesium level was 1,99±0.36 mEq/L. Among total 56 patients, 15 patients (26.8%) showed hypermagnesemia (serum magnesium >2.2 mEq/L) and 5 patients (8.9%) showed hypomagnesemia (serum magnesium <1.6 mEq/L). Among all 56 patients, serum iPTH (intact PTH) level was not correlated with serum magnesium level. However, it was inversely correlated with serum total calcium and ionized calcium levels, respectively (r = − 0.365, p = 0.006; r = − 0.515 p < 0.001). Among 49 patients whose serum iPTH level was less than 300 pg/mL, serum iPTH level was inversely correlated with serum magnesium level (r = − 0.295, p=0.039) and inversely correlated with serum total calcium and ionized calcium levels, respectively (r = − 0.546, p < 0.001; r = − 0.572 p < 0.001). Among 49 patients whose serum iPTH level was less than 300 pg/mL, lower iPTH group (serum iPTH < 120 pg/mL) showed higher serum magnesium level (p = 0.037), higher serum total calcium level (p < 0.001) and lower bone isoenzyme of alkaline phosphatase level (p < 0.001) than those of higher iPTH group (120 pg/mL≤serum iPTH < 300 pg/mL).ConclusionAmong the CAPD patients whose serum iPTH level was less than 300 pg/mL, there was a significant inverse correlation between serum iPTH level and serum magnesium level. This study indicates that not only serum calcium level but also serum magnesium level are important in the regulation of serum iPTH levels of CAPD patients who have been dialyzed by low-magnesium peritoneal dialysate.

Familial isolated hyperparathyroidism: clinical and genetic characteristics of 36 kindreds.

Familial isolated hyperparathyroidism: clinical and genetic characteristics of 36 kindreds.

High Prevelance of Chronic Magnesium Deficiency in T Cell Lymphoblastic Leukemia and Chronic Zinc Deficiency in Children with Acute Lymphoblastic Leukemia and Malignant Lymphoma

Magnesium and zine are the elements having essential roles in regulation of cell growth, division and differentiation. There have been some studies in the literature suggesting an association between the deliciency of these elements and the development of malignant disorders. In this study hair and serum Zine and magnesium levels were investigited in children with acute lymphoblastic leukemia (ALL) and malignant lymphoma (ML) at the time of initial diagnosis. Ten children with T-cell ALL. 10 children with B-precursor ALL. 5 children with Burkitt's Lymphoma (BL). II children with Hodgkin's lymphoma (HL). 10 children with non-Burkitt non-Hodgkin's lymphoma (NBNHL) and 12 age and sex matched healthy children as a control group were included in the study. Mean hair magnesium levels in all of the groups of the patients were lower than the levels in the control group but the difference was statistically significant only in the children with T cell ALL comparable to the controls (28.9±3.9μg/g and 87.6±18.5μg/g respetiveley, p<0.05). Mean serum magnesium levels in all the cohorts were not significantly different than those in controls (p>0.05 in each comparison). Mean hair zine levels in the patients with T-cell. B-precursor ALL, BL, HL, NBNHL were 103.4±14.6μg/g. 100.9±7.8μg/g. 91.1±19μg/g, 72.5±9.1μg/g. 103.2±12.2μg/g respectively. Each of these levels were significantly lower than the mean hair Zine levels of the control group (141.2±9.6μg/g. p<0.05 in each comparison). Although mean serum zine levels in all of the groups were also decreased, the differences were statistically significant only in the groups with B-precursor ALL. HL and NBNHL (75.9±5.29μg/dl. 68.6±7.3mUg/dl. 85.7±5.5μg/dl respectively) when compared with controls (105.1±9.9μg/dl, p<0.05 in each comparison). Hair magnesium and zine levels showed a positive correlation with each other in all the groups (r≅0.5). No significant difference was found in the mean hair/serum magnesium and Zine levels between malnourished and nonmalnourished patients.In conclusion, regarding the results of our study and previous daia in the literature chronic magnesium and zine deficiency seems to be associated with the development of ALL and malignant lymphoma in a group of patients.

Effects of magnesium sulfate tocolysis on maternal mental status

Objective: Magnesium sulfate is the most commonly used agent for tocolysis in the management of preterm labor. Anecdotally both clinicians and patients have noted alterations in mental status of women receiving high doses of magnesium infusion, and central nervous system depression including lethargy and depression of deep tendon reflexes has been documented. Our hypothesis is that intravenous magnesium sulfate at tocolytic doses significantly affects maternal mental status. Materials and Methods: Eligibility criteria included admission or transport to University Hospital between 25 and 34 weeks gestation with an initial episode of spontaneous premature labor. Patients were consented and given an initial mental status examination prior to magnesium sulfate infusion. Those patients transported to University Hospital diagnosed with premature labor and already on magnesium were consented and given an initial mental status examination at the time of arrival. Once a therapeutic level of magnesium was documented a repeat mental status examination was performed, with a third examination performed 24 hours after the magnesium infusion has been discontinued. As a control group pregnant women hospitalized for premature rupture of the membranes not in labor had the examinations performed initially, after 24 hours of hospitalization, and again after 72 hours of hospitalization. Exclusion criteria included underlying mental illness, administration of other medications that might affect mental status, cervical dilation greater than 4 cm, clinical evidence of chorioamnionitis, or the presence of any significant abnormalities in the fetal heart rate tracing. The mental status examination consisted of the mini mental state exam, the comprehension portion of the Wechsler Adult Intelligence Scale, and the Bender-Gestalt Indicator. The results of these examinations were scored in a blinded fashion by a psychiatrist. Results: There were 22 patients in the study group and 9 patients in the control group. There were no differences in the age, gravidity, parity, or gestational age of the two groups. Out of a possible 102 points, the mean mental status scores were as follows: Initial Therapy Final P Value MgSO 4 76.3 ± 11.2 74.7 ± 12.2 79.3 ± 14.6 .66 Control 78.7 ± 13.1 77.9 ± 11.9 76.3 ± 12.7 .64 The mean serum magnesium level at the time of therapy was 5.1 mg/dL. The time required for response to the Wechsler test was significantly different although the scoring of the comprehension was unchanged (15.2 ± 3.6 min vs 22.3 ± 4.7 min, P < .05). Conclusions: This prospective blinded study reveals no differences in maternal mental status during magnesium sulfate infusion at the levels recorded in our study. There was an increase in the length of time required to answer the comprehension and judgment portion of the examination. These findings have significant clinical implications suggesting that patients on magnesium sulfate can make appropriate judgments and can, therefore, participate in clinical discussions and trials.

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.

Effect of intravenous magnesium sulfate on the biophysical profile of the healthy preterm fetus

OBJECTIVE: The null hypothesis is that intravenous magnesium sulfate does not affect the biophysical profile of the healthy preterm fetus. STUDY DESIGN: Thirty-one fetuses of 25 patients between the gestational ages of 24 and 35 weeks, median 31.4 and mean (± SD) 30.4 (± 2.9), who required tocolysis for uterine contractions were prospectively studied. After normal fetal biophysical assessment was documented, intravenous magnesium sulfate was started as a 4 or 6 gm loading dose and then infused at 2 to 3.5 gm/hr to achieve tocolysis. Blood was drawn for measurement of maternal serum magnesium levels immediately before intravenous magnesium sulfate was administered and at 2 and 12 hours after the loading dose. Biophysical profiles, consisting of a possible 12 points, were performed at the same time as blood was drawn. Serum magnesium levels were compared with one-way analysis of variance for repeated measures and biophysical profile scores with Friedman's test. Statistical significance was considered p < 0.05. RESULTS: Mean (± SD) serum magnesium levels were 1.7 (± 0.1) mg/dl before infusion, 4.3 (± 0.6) mg/dl at 2 hours, and 5.2 (± 0.7) mg/dl at 12 hours (p < 0.001). Six fetuses did not have a 12-hour biophysical profile; three were delivered for severe variable decelerations, two progressed in labor, and in one tocolysis was discontinued. The median biophysical profile score was 11 before intravenous magnesium sulfate, at 2 hours, and at 12 hours after the loading dose. The biophysical parameters present and the percentage of fetuses with each parameter were as follows: breathing (>30 seconds), 88% (22/25) before magnesium sulfate, 84% (21/25) at 2 hours, and 92% (23/25) at 12 hours; nonstress test (reactive), 84% (21/25) before magnesium sulfate, 68% (17/25) at 2 hours, and 80% (20/25) at 12 hours; movement (normal), 100% (25/25) before magnesium sulfate, 100% (25/25), at 2 hours, and 96% (24/25) at 12 hours; tone (normal), 100% (25/25) before magnesium sulfate, 100% (25/25) at 2 hours, and 96% (24/25) at 12 hours. CONCLUSION: Intravenous magnesium sulfate did not significantly alter the biophysical profile in the 25 fetuses evaluated by three biophysical profiles in spite of the significant increase in maternal serum magnesium levels. (AM J OBSTET GYNECOL 1994;170:1131-5.)

Seasonal Hypomagnesemia in reindeer on Kautokeino winter pasture in Finnmark County, Norway

Hypomagnesemia was diagnosed in reindeer on Kautokeino winter pasture in Finnmark County, Norway. The affected animals were paretic or ataxic. Mean serum magnesium levels were 0.19 +/- 0.20 mm/L (n = 6), compared to a serum Mg level of 0.82 +/- 0.17 mm/L for the reference group.

Serum and Rectal Mucosal Magnesium Status in Acute and Chronic Diarrhoea

Serum and rectal mucosal magnesium content was estimated in children (6-18 months old) with acute diarrhoea (Group I: n = 50), chronic diarrhoea (Group II: n = 25), extra-intestinal infections (Group III: n = 15) and healthy controls (Group IV: n = 20). The sex and nutritional status of the different groups were comparable. The mean serum magnesium levels in acute and chronic diarrhoea were comparable to healthy and infected controls. The tissue magnesium content of infants with chronic diarrhoea was significantly (P less than 0.001) lower than other groups. Repeat estimation at discharge in 38 patients (25 in Group I, 13 in Group II) revealed a significant reduction in serum levels in both groups (P less than 0.05 and P less than 0.01, respectively) and in tissue levels in acute diarrhoea (P less than 0.05). A total of 23 infants (16 in Group I) were evaluated 2-3 weeks after discharge. There was an increase in tissue magnesium content at recovery in acute (P less than 0.02) and chronic (P greater than 0.05) diarrhoea groups. It is concluded that infants with chronic, but not acute diarrhoea, are magnesium depleted at presentation; with the continuation of diarrhoea there is a progressive depletion of magnesium; and there is a tendency to regain the magnesium status during the convalescent period.

Prospective Study on Premature Labor with Magnesium Sulfate

The efficacy of magnesium sulfate was evaluated as the primary tocolytic agent in the management of patients at risk for premature delivery. Fifteen patients presenting with premature labor between 28 and 35 weeks gestation, given titrated dose intravenously magnesium sulfate till uterine contraction ceased, were prospectively studied. All patients received an additional oral beta-mimetic agent once labor was arrested till 36 weeks gestation. All cases had intact membranes and no contraindications for tocolytic therapy. Tocolysis for more than 72 hours was achieved in 14 cases (93.3%). Delayed tocolysis of more than 7 days was achieved in 13 cases (86.7%). The mean dosage to achieve tocolytic effect was 3.17 g/hr (SD 0.08). The mean serum magnesium level to achieve such effect was 5.38 mg/dl (SD 0.88). Magnesium sulfate was found to be easy to administer and clinically efficacious with minimal adverse effects. It may be used as the first line of tocolytic therapy where beta-sympathomimetic drugs are contraindicated.

Magnesium tocolysis: Serum levels versus success

The relationship between maternal serum magnesium levels and tocolytic success is poorly established. We performed a retrospective analysis of 101 episodes of preterm labor treated with magnesium sulfate and compared the initial, average, and maximum serum magnesium levels with tocolytic success at 48 hours and 7 days. There was no difference in the proportions of tocolytic success when serum levels were less than 6 mg/dl compared with levels of greater than or equal to 6 mg/dl. Similar analyses on either side of 5 mg/dl also revealed no significant relationship. Mean serum magnesium levels in patients with successful tocolysis were statistically similar to those of patients in whom tocolysis failed. Multiple logistic regression analysis also failed to establish a positive relationship between serum magnesium levels and tocolytic success. We conclude that serum magnesium levels alone should not serve as an end point of therapy.

Parenteral magnesium sulfate fails to control electroshock and pentylenetetrazol seizures in mice

Magnesium sulfate has been used as an anticonvulsant in the treatment of eclampsia, but efficacy of magnesium in other types of seizure disorders is poorly documented. We examined the effects of magnesium sulfate (MgSO 4) on seizures produced in mice by maximal electroshock (MES) and pentylenetetrazol (PTZ). MgSO 4 injection (6.7 mEq/kg i.p.) caused weakness in all animals. With supra-threshold electroshock, 10 10 controls and 11 12 treated animals had seizures with tonic hind limb extension ( P = NS). Electroshock threshold was unaltered by magnesium treatment ( n = 48; P = 0.47). PTZ induced clonic seizures in 12 12 controls and 5 14 treated animals ( P < 0.05). This difference was likely due to muscular weakness because frequency of EEG spikes was the same in PTZ and PTZ + MgSO 4 groups. Mean serum magnesium levels were 2.3 ± 0.3 mEq/1 in animals not given MgSO 4; 10.9 ± 1.4 mEq/1 and 12.8 ±2. mEq/1 in treated animals with and without seizures ( P = NS). We conclude that magnesium sulfate had no significant anticonvulsant activity in mouse MES and PTZ models for epilepsy. The relevance of these findings to the possible efficacy of magnesium sulfate in eclamptic seizures and other types of epilepsy remains to be determined.

Hypomagnesemia and Hypertension in Primary Hyperparathyroidism

A retrospective study of 89 patients with surgically proven primary hyperparathyroidism was done to gain insight into the pathogenesis of hypertension associated with this condition. The 43 patients (48%) who were hypertensive did not differ significantly from the normotensive patients with regard to age, sex, serum calcium and phosphate levels, and creatinine clearance. However, the mean serum magnesium level was significantly lower in hypertensive hyperparathyroid patients (1.52 +/- 0.24 mEq/L) than in normotensive hyperparathyroid patients (1.76 +/- 0.18 mEq/L; P less than .001), irrespective of use of diuretics in the former group. Although some studies implicate hypomagnesemia in the pathogenesis of essential hypertension, we are unaware of any previous human study reporting a link between hypomagnesemia and hypertension associated with primary hyperparathyroidism. This study suggests that a low level of serum magnesium may play a role in the pathogenesis of hypertension associated with primary hyperparathyroidism, a finding that needs further evaluation.

Renal handling of magnesium in transplanted children under cyclosporin A treatment.

We investigated the renal handling of magnesium in 12 transplanted children under cyclosporin A treatment during the early period after transplantation. We also studied 30 children treated with cyclosporin A 2 years after renal transplantation and compared the results with those of 22 children treated with azathioprine and prednisolone 2-4 years after transplantation. Twenty-two children with chronic renal failure and 10 healthy children served as controls. During the 1st week after transplantation, the mean serum magnesium level dropped to 0.54 +/- 0.14 mmol/l and was accompanied by a high fractional magnesium clearance. During this period two patients showed generalized convulsions. After magnesium substitution, serum levels increased gradually and normalized 4 months later. Fractional magnesium clearance remained slightly elevated due to lower glomerular filtration rates. One to four years after transplantation there were no statistically significant differences in serum levels, clearance, excretion and fractional clearance of magnesium between patients treated with cyclosporin A and those receiving azathioprine. There was a linear regression between magnesium clearance and creatinine clearance and an inverse exponential correlation between fractional magnesium clearance and creatinine clearance. We conclude that cyclosporin A treatment after transplantation has no major effect on the renal handling of magnesium in kidney transplants. The observed changes in serum magnesium levels and fractional clearance are probably due to tubular cell damage early after transplantation and to high doses of furosemide.