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Despite the presumption of a beneficial effect of magnesium (Mg) supplementation on various diseases, little is known concerning the pharmacokinetics of Mg hydroxide. This study was designed to provide a pharmacokinetic profile of Mg hydroxide after a single oral dose. Ten healthy male adults participated in this cross-over study with three 24-hr study days. Interventions were (i) none (baseline), (ii) oral intake of three (3 × 360 mg) tablets of Mg hydroxide (Mablet ® ) and (iii) IV bolus infusion of 2 g Mg sulphate (index drug). Blood samples were collected before the single dose, after (i.e. after treatment administration) 15, 30, 60, 90 and 120 min. and after 3, 4, 6, 8, 12 and 24 hr. Urine was collected in four 6-hr periods per study day. Blood (N = 10) and urine (N = 6) Mg were analysed by descriptive statistics. Bioavailability was 14.9% (CI: 8.3; 26.8), blood clearance was 5.1 L/hr (CI: 2.1; 17.0), apparent volume of distribution was 60.2 L (CI: 35.6; 102.0), elimination constant was 0.08 per hour (CI: 0.05; 0.14), half-life was 8.3 hr (CI: 4.8; 14.1), C max was 0.11 mmol/L (CI: 0.07; 0.14), and AUC [0-24] was 92.3 mmol/L × min. (CI: 45.5; 139.1). Urine Mg excretion augmented by 17.7% (CI: 8.9; 35.0) from baseline. No severe side effects were observed. The bioavailability of Mg hydroxide was 15%, and it constitutes a clinically relevant option for oral Mg supplementation. No severe side effects were seen., (© 2016 Nordic Association for the Publication of BCPT (former Nordic Pharmacological Society).)

The possible influence of Maalox 70, an antacid based on magnesium-aluminum hydroxide, and the H2-antagonist cimetidine, both commonly prescribed in hypercholesterolemic patients, on the pharmacokinetics of the new HMG-CoA reductase inhibitor cerivastatin was investigated in 2 separate studies in 8 healthy young male subjects each. Cerivastatin plasma concentration/time profiles were assessed by a specific HPLC assay; in addition, total immunoreactive drug (cerivastatin plus metabolites) was determined by RIA. Single oral doses of 200 micrograms cerivastatin were administered under fasting conditions without or with 10 ml Maalox 70 suspension. The mean AUC and Cmax ratios (combined dosing/monodosing) including 90% confidence intervals were 0.92 (0.73-1.15) and 0.89 (0.72-1.10) for the HPLC data, and 0.99 (0.85-1.14) and 1.03 (0.82-1.30) for the RIA data, respectively. Thus, no interaction of the simultaneous administration of Maalox 70 on the pharmacokinetics of cerivastatin was observed. In a similar controlled, randomized nonblind 2-way crossover design the influence of the H2- antagonist and well-known cytochrome P450 enzyme inhibitor cimetidine was investigated. Eight healthy young male volunteers received single oral doses of 200 micrograms cerivastatin alone or on the fourth day of a 4-day cimetidine 400 mg b.i.d. pretreatment. The mean AUC and Cmax ratios (combined dosing/monodosing) including 90% confidence intervals were 0.98 (0.90-1.08) and 0.91 (0.78-1.07) for the RIA data, and 0.89 (0.82-0.96) and 0.93 (0.80-1.09) for the HPLC data, respectively, clearly indicating that cimetidine and cerivastatin did not interact pharmacokinetically. These results do not only reflect the apparent insensitivity of cerivastatin absorption to possible changes in gastric pH, but demonstrate that the metabolic pathways of cerivastatin, involved in its first-pass metabolism and elimination, are rather insensitive to cytochrome P450 enzyme inhibition induced by cimetidine.

This is a case of magnesium intoxication in a neonate produced by an oral magnesium cathartic. A review of the literature revealed there are very few cases that have been reported of magnesium toxicity due to cathartics. There is no recommended dose for magnesium cathartics in neonates or data on their safety. A review of the management of magnesium intoxication is presented.

In a double-blind, placebo-controlled study, 47 patients with ischemic heart disease and acute myocardial infarction were allocated to 3 months' treatment with peroral magnesium (15 mmol/d) or placebo. Before, during, and after treatment, blood samples were taken to determine serum concentrations of cholesterol; triglyceride; high-density, low-density, and very-low-density lipoprotein; apolipoprotein A1 and B; and magnesium. We found a 13% increase in molar ratio of apolipoprotein A1:apolipoprotein B after magnesium treatment, as compared with a 2% increase in the placebo group (for mean differences between changes of the magnesium and the placebo groups). This increase was caused by a decrease in apolipoprotein B concentrations, which were reduced by 15% from 1.44 to 1.23 mmol/L in the magnesium group as compared with a slight increase in the placebo group. Triglyceride, and thereby very-low-density lipoprotein concentrations decreased by 27% after magnesium treatment (from 2.41 to 1.76 mmol/L, and from 1.1 to 0.79 mmol/L, respectively) as compared with much smaller decrements in the placebo group. Likewise, we found tendencies toward an increase in high-density lipoprotein cholesterol and in high-density lipoprotein cholesterol ratio/(low-density lipoprotein cholesterol:very-low-density lipoprotein cholesterol) after magnesium treatment. The observed findings support the hypothesis that magnesium deficiency might be involved in the pathogenesis of ischemic heart disease by altering the blood lipid composition in a way that disposes to atherosclerosis.

We studied the serum aluminum levels of 30 intensive care patients receiving six daily doses of magaldrate (Riopan) or aluminium hydroxide (Trigastril). In both groups we found a significant rise of the serum aluminium concentration (p less than 0.01) following administration of the antacid solutions. Examination on day 9 and 15 the magaldrate group showed significantly (p less than 0.05) lower aluminium levels than the aluminium hydroxide group. An increase up to the critical serum aluminium level of 100 ng/ml occurred in none of the patients that all had normal or slightly impaired renal function. Therefore routine measurements of serum aluminium levels in patients without renal impairment are not considered necessary following antacid therapy. However, we recommend the use of antacids with an aluminium absorption rate as low as possible.