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At least 91 records · Page 5Linked to original sources
PubMed1988

Magnesium hydroxide as a complementary aluminium-free phosphate binder to moderate doses of oral calcium in uraemic patients on chronic haemodialysis: lack of deleterious effect on bone mineralisation.

To control hyperphosphataemia without hyperaluminaemia, A1(OH)3, which was given in addition to high doses of oral calcium, was replaced by Mg(OH)2 for 6 months in 20 haemodialysed patients and for 20 months in 12. The treatment during the control period was 110 +/- 91 mmol/day of oral calcium element given as CaCO3 and/or Calcium Sorbisterit and 1.05 +/- 1.47 g/day of A1(OH)3. Haemodialysis treatment was 4 h, thrice weekly. To prevent hypermagnesaemia, dialysate magnesium was decreased from 0.75 mmol/l to 0.375 mmol/l. After a control period of 3 months, Mg(OH)2 was given at a mean dose of 2.6 +/- 2 g/day and oral calcium supplements were decreased to 76 mmol/day. Two subsequent bone histomorphometry studies were performed at 8 month intervals in four patients and at 20 month intervals in seven patients. The results show a good control of plasma calcium (mean +/- SD: 2.43 +/- 0.1 mumol/l); phosphate (1.76 +/- 0.4 to 1.66 +/- 0.3 mmol/l); aluminum (1.3 +/- 0.1 mumol/l to 0.6 +/- 0.1 mumol/l); alkaline phosphatase (135 +/- 65 to 125 +/- 40 IU); and PTH fragments (PTH C terminal decreased from 260 +/- 214 to 185 +/- 182 pg/ml, PTH medium from 4185 +/- 5113 to 2270 +/- 4880 pg/ml). Plasma magnesium increased from 0.96 +/- 0.2 to 1.54 +/- 0.2 mmol/l. Bone histomorphometry shows no change in mineralisation, and a borderline decrease of resorption parameters. The main side-effects are (1) diarrhoea, which was well controlled by transient treatment with karaya gum, and (2) an increased need for potassium binders.(ABSTRACT TRUNCATED AT 250 WORDS)

Bone and Bones↗
PubMed1992

Magnesium hydroxide: new insights into the mechanism of its laxative effect and the potential involvement of prostaglandin E2.

The mechanism by which Mg(OH)2 acts as a laxative is unknown. To explore the mechanism, six volunteers more than 55 years old, with normal bowel habits, were enrolled in a dose-response, randomized, placebo-controlled, double-blind, crossover design study. Each subject was studied for four inpatient periods of 5 days each on a metabolic ward with 9 days off of all medication between studies. In the hospital, all patients were on a diet fixed in calories, fluid volume, Na+, fiber, and Ca2+. At 8 p.m. on each study day, each subject took 45 ml containing either placebo or 1,200, 2,400, or 3,600 mg of Mg(OH)2 plus 240 ml of water. On the fourth and fifth hospital days of each period, 24-h stool output was quantified and analyses performed. Compared to placebo, Mg(OH)2 caused the following dose-dependent results: (a) increased number of bowel movements; (b) increased percentage of stool water; (c) increased stool volume; (d) increased stool Mg2+; and (e) increased total stool 24-h prostaglandin E2 (PGE2), with mean 24-h excretions as follow: placebo, 95 +/- 18 pg/24 h; 1,200 mg Mg(OH)2, 260 +/- 100; 2,400 mg Mg(OH)2, 357 +/- 117; and 3,600 mg Mg(OH)2, 525 +/- 196. There was a significant correlation between stool PGE2 excretion and stool water consistent with a causative relationship. However, the concentration of stool prostaglandin was lower than the concentration found to alter intestinal electrolyte transport in vitro. In summary, the laxative effect of Mg(OH)2 is associated with increased output of stool PGE2. The contribution of the stool PGE2 to the laxative effect of Mg(OH)2 is unknown.

Cathartics↗
PubMed1977

The effect of an antacid on the bioavailability of indomethacin.

The biovailability of indomethacin from two indomethacin-antacid (aluminum hydroxide magnesium carbonate and magnesium hydroxide) combinations was compared with the bioavailability of oral indomethacin. Relative bioavailability was estimated by three methods: comparison of plasma concentrations at various times, comparison of areas under plasma concentration time curves, and comparison of the amount of drug excreted unchanged in the urine. A double blind three-way crossover study was conducted in twelve healthy volunteers. The combination with the slightly smaller amount of antacid (preparation A) showed significantly decreased bioavailability by all three methods in comparison with indomethacin alone (preparation C). The combination with the larger amount of antacid (preparation B) was also less bioavailable than preparation C. This effect was significantly only for the comparison of areas under curves and not for plasma levels, although the mean plasma levels produced by preparation B at all times were lower than those for preparation C. These findings suggest that aluminum hydroxide magnesium carbonate and magnesium hydroxide decrease the bioavailability of indomethacin.

Adult↗
PubMed1983

Antacid effects on the gastrointestinal absorption of riboflavin.

The effect of aluminum hydroxide, magnesium hydroxide, and a combination of aluminum-magnesium hydroxide suspensions on the oral absorption of riboflavin was examined in five subjects. Coadministration of aluminum hydroxide or magnesium hydroxide suspension with riboflavin (30 mg) resulted in an increase in time of peak urinary excretion rate of riboflavin when compared with control studies. There was no increase in the peak excretion rate or total urinary excretion of riboflavin when the antacid-treated subjects were compared to the control studies. In vitro experiments indicated that significant binding of riboflavin to the aluminum hydroxide and magnesium hydroxide suspensions occurred. The results of the present investigation are consistent with the reported effect of aluminum ion on GI motility and the known influence of gastric emptying on the absorption of riboflavin from the GI tract.

Adult↗
PubMed1994

Enhancement of drug absorption by antacids. An unrecognised drug interaction.

Antacids are widely used for many disorders. The potential of antacids to interact with other concomitantly ingested drugs is well recognised. These interactions usually result in reduced or delayed absorption of the affected drug. However, this is not always the case. In contrast to aluminium hydroxide, magnesium hydroxide and sodium bicarbonate can enhance the absorption of some drugs. For example, magnesium hydroxide can increase the rate and sometimes even the extent of absorption of certain nonsteroidal anti-inflammatory drugs (e.g. tolfenamic acid, mefenamic acid and ibuprofen), sulphonylurea antidiabetic agents [e.g. glipizide, glibenclamide (glyburide) and tolbutamide] and the oral anticoagulant dicoumarol (bishydroxycoumarin). These weakly acidic drugs are nonionised at gastric pH, but are sparingly water soluble. Elevation of the gastric pH by administration of magnesium hydroxide or sodium bicarbonate increases the solubility and absorption of such sparingly water soluble agents. Chelate formation may be involved in the increased absorption of dicoumarol by magnesium hydroxide. In combination antacids containing both aluminium hydroxide and magnesium hydroxide, the absorption enhancing effect of magnesium hydroxide seems to be counterbalanced by the opposing effects of aluminium hydroxide. The clinical significance of increased drug absorption is not clear. However, accelerated and enhanced absorption of analgesic drugs may be beneficial when rapid pain relief is desired. In contrast, an unexpectedly increased hypoglycaemic or anticoagulant effect may be potentially dangerous. Therefore, a knowledge of the potential effect of antacids on the absorption of other drugs is clinically important.

Absorption↗