Clinical evaluation of pemoline and magnesium hydroxide as a mild stimulant in geriatric patients.
Explore the source record for details and available documents.
Aged↗
SEARCH · Search PubMed
Results for “Magnesium Hydroxide”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Pemoline and magnesium hydroxide versus pemoline: enhancement of learning and memory of a conditioned avoidance response in rats.
Explore the source record for details and available documents.
Animals↗
Effects of magnesium salts in preventing experimental oxalate urolithiasis in rats.
Magnesium oxide, magnesium hydroxide, magnesium sulfate, magnesium trisilicate, and magnesium citrate were added to a calcium-oxalate lithogenic diet in order to determine their effects in preventing lithogenesis. Male Wistar-strain rats which had been fed the glycolic-acid diet developed marked urinary calculi within four weeks. Rats in the magnesium-hydroxide, magnesium-citrate, and magnesium-trisilicate groups, however, had almost no stones in the urinary system. Rats in the magnesium-oxide and magnesium-sulfate groups showed significantly less effect than those in the former three groups. During the experimental period, the 24-hour urinary oxalate excretion and concentration were higher in the glycolic-acid group than in the other groups. The urinary citrate excretion and concentration were the highest in the magnesium-hydroxide and magnesium-citrate groups and higher in the magnesium-trisilicate and magnesium-oxide groups than in the magnesium-sulfate and glycolic-acid groups. Similar trends were observed in the urinary magnesium excretion and in its concentration. The urinary calcium excretion and concentration were higher in the experimental groups than in the glycolic-acid group. The urinary calcium/magnesium ratio remained mostly unchanged. Therefore, it can be concluded that alkaline magnesium salts increase the urinary calcium and magnesium concentrations, without changing the calcium/magnesium ratio, and inhibit urinary calculi formation, most likely by increasing the urinary citrate concentration.
Animals↗
Synthesis and Structure of a Magnesium Hydroxide Complex Supported by Tris(pyrazolyl)hydroborato Ligation, {[Tp(Ar,Me)]Mg(&mgr;-OH)}(2) (Ar = p-Bu(t)C(6)H(4)).
Explore the source record for details and available documents.
Journal Article↗
Amphiphilic templating of magnesium hydroxide.
The synthesis of lamellar mesostructured Mg(OH)2 was achieved through a surfactant templating route. Amphiphilic compounds with different anionic headgroups (phosphate, sulfate, sulfonate, and carboxylate) were used as surfactants. Control of d spacing was achieved through the use of different alkyl carboxylate amphiphiles. It is proposed that the interaction between the highly reactive oxygen atoms of the anionic surfactants and the highly electrophilic Mg atom leads to the formation of high charge density at the interface between the surfactant molecules and the inorganic precursor. This interaction is very strong and the existence of strong bonds between the headgroup molecules of the surfactant and the Mg atom locks the structure in a preferred orientation, i.e., lamellar mesostructure. The strong interaction thus precludes any phase transformation, and only the lamellar phase of Mg(OH)2 is obtained. Calcination of the surfactant by heating in oxygen flow leads to the collapse of the lamellar mesophase and results in the formation of nonporous MgO.
Journal Article↗
Interactions between ciprofloxacin and antacids--dissolution and adsorption studies.
Ciprofloxacin is a fluorinated quinolone antibacterial agent extensively used against both Gram-positive and Gram-negative microorganisms. In certain polytherapy programs, ciprofloxacin can be administered with some antacids that could modify its dissolution rate and reduce its absorption leading to therapeutic failure. The aim of this study was to evaluate the influence of some antacids on the availability of ciprofloxacin. The release of ciprofloxacin from tablets in the presence of antacids, such as sodium bicarbonate, calcium hydroxide, calcium carbonate, aluminum hydroxide, magnesium hydroxide, magnesium carbonate, magnesium trisilicate and magaldrate was studied on BP 2002 dissolution test apparatus. These studies were carried out in simulated gastric and intestinal juices for 3 hours at 37 degrees C. The results confirmed that the dissolution rate of tablets was markedly retarded in the presence of all the antacids studied. Magaldrate and calcium carbonate in simulated gastric juice exhibited relatively higher adsorption capacities, as did magnesium trisilicate and calcium hydroxide in simulated intestinal juice.
Adsorption↗
Interactions between sparfloxacin and antacids - dissolution and adsorption studies.
Sparfloxacin is a broad-spectrum oral fluoroquinolone antimicrobial agent with a long elimination half-life, extensively used against both Gram-positive as well as Gram-negative microorganism. Concurrent administration of antacids and sparfloxacin decreases the gastrointestinal absorption of sparfloxacin and therapeutic failure may result. The present study was designed to evaluate the influence of some antacids on the availability of sparfloxacin. The release of sparfloxacin from tablets in the presence of antacids like sodium bicarbonate, calcium hydroxide, calcium carbonate, aluminum hydroxide, magnesium hydroxide, magnesium carbonate, magnesium trisilicate and magaldrate has been studied on BP 2003 dissolution test apparatus. These studies were carried out in simulated gastric and intestinal juices for three hours at 37 degrees C. The results confirmed that the dissolution rate of tablets was markedly retarded in the presence all of antacids studied, whereas magaldrate and calcium carbonate exhibited relatively higher adsorption capacities in simulated gastric juice and magnesium trisilicate and calcium hydroxide in simulated intestinal juice.
Adsorption↗
In vitro monitoring of ciprofloxacin antacids interactions by UV & HPLC.
Ciprofloxacin or 1-cyclopropyl-6-fluoro-1,4-dihydro-4-oxo-7-(1-piperazinyl]-3-quinoline carboxylic acid is a fluorinated quinolone antibacterial agent extensively used worldwide. There are number of drug interactions reported for this antibacterial agent. In present studies, in vitro release of ciprofloxacin hydrochloride in presence of various antacids like sodium bicarbonate, calcium hydroxide, calcium carbonate, aluminum hydroxide, magnesium hydroxide, magnesium carbonate, magnesium trisilicate and magaldrate has been studied on BP 2002 dissolution test apparatus. Drug in each case was analyzed either by measuring the absorbance of aliquots at 278 and 316 nm on a UV/VIS spectrophotometer, or by reversed-phase high-performance liquid chromatographic (RP-HPLC) method. These studies were carried out in simulated gastric and intestinal juices for three hours at 37 degrees C. The availability of ciprofloxacin was found to be markedly retarded in presence of all the antacids studied.
Adsorption↗
Pancreatic enzyme replacement: the effect of antacids or cimetidine.
The effect of the addition of sodium bicarbonate, aluminum hydroxide, magnesium hydroxide, calcium carbonate, or cimetidine to supplemental pancreatic enzyme therapy was investigated in patients with severe exocrine pancreatic insufficiency. Steatorrhea was reduced with the administration of three enzyme tablets with meals (73 vs 29 g/24 hr). The coadministration of enzyme tablets with either sodium bicarbonate (16.6 g/24 hr, P = 0.08), or aluminum hydroxide (18.4 g/24 hr, P = 0.029) yielded a greater reduction in steatorrhea than enzymes alone (29 g/24 hr). Neither magnesium-aluminum hydroxide (36.3 g/24 hr, P = 0.22), nor calcium carbonate (39.0 g/24 hr, P = 0.029), improved efficacy of enzyme therapy and, in fact, tended to enhance steatorrhea. With the administration of cimetidine there was no significant effect on steatorrhea compared to enzymes alone (32.1 vs 29 g/24 hr, P greater than 0.3). Intraduodenal lipase activity following test meals was found to be a poor predictor of the effectiveness of antacid therapy in improving the efficacy of supplemental enzymes.
Adult↗
Adsorption of bile acids by sucralfate, antacids, and cholestyramine in vitro.
Sucralfate, one of the newer drugs shown to be effective in the treatment of peptic ulcer and esophagitis; cholestyramine, a known bile acid binder; and commercial antacid preparations of pure aluminum hydroxide, pure magnesium hydroxide, and a combination of aluminum hydroxide, magnesium hydroxide, and magnesium carbonate were tested in vitro for bile acid-binding capacity. Cholestyramine was found to be the most effective bile acid binder, with more than 90% of bile acids adsorbed at all of the pH values studied. Sucralfate proved efficacious at pH 4, 6, and 8, adsorbing about 50% of the bile acids, but its binding capacity decreased at pH 2. Pure aluminum hydroxide was the most effective of the various antacid preparations; it adsorbed about 90% of bile acids at pH 2, although this percentage was significantly reduced at pH 6 and 8. Sucralfate was significantly more effective as a bile acid absorbent at pH 4 than either the magnesium hydroxide or aluminum-magnesium hydroxide plus magnesium carbonate antacids, as effective as the aluminum hydroxide antacid, and significantly less effective than cholestyramine.
Adsorption↗
Evaluation of antacid tablets and liquid in fasting and fed men and women.
In view of in vitro tests suggesting good performance of an experimental tablet formulation of an aluminum hydroxide-magnesium hydroxide antacid, a study was conducted to evaluate the efficacy in vivo. Twenty-three healthy men and women were enrolled in the study, which was carried out in two parts: fasting and postprandial. Eight of the volunteers failed to qualify because of repeated baseline pH greater than 2.5. In the 15 participants who qualified, the intragastric pH was monitored for up to 240 minutes after the administration of one or two experimental tablets, 5 or 10 ml of a commercially available liquid antacid, or placebo. In the fasting subjects (n = 10), the antacids rapidly increased the mean pH. One antacid tablet and 5 ml of liquid antacid yielded similar results, with mean peak pH values of 5.2 and 4.8 and durations above pH 3.5 of 25 and 40 minutes, respectively. When the doses were doubled, 10 ml of liquid produced a peak pH of 6.7 and maintained the pH above 3.5 for 40 minutes, whereas two tablets produced a peak pH of 4.8 and maintained pH above 3.5 for 15 minutes. In the fed subjects (n = 10), neither antacid formulation at either dose significantly raised intragastric pH. Further studies are needed to establish the optimal time for postprandial administration of antacids.
Adult↗
Studies on the in vitro interactions of cimetidine with commercial antacid preparations and chemically pure components.
Studies of the in vitro binding of cimetidine to commercial antacid preparations such as colloidal aluminium hydroxide-magnesium hydroxide, aluminium hydroxide-calcium carbonate and the chemical pure components Al(OH)3, Mg(OH)2 or Al2O3 showed no adsorption of cimetidine at cimetidine to antacid ratios employed in clinical practice. Small degrees of binding were observed with two silicate containing antacids (21.4 +/- 0.5 mumol/g and 12.3 +/- 1.9 mumol/g).
Adsorption↗
Effect of food on antacid neutralizing capacity in man.
In order to estimate their in-vivo reactivity two antacids of equal theoretical neutralizing capacity (approximately 3.9 mol/l at pH 3.5) but of different chemical composition were employed as intragastric titrant (pH 3.5) following a liquid protein meal (oxo) in two groups of five volunteers each. The two antacids chosen (alucol and Camalox) contain different amounts of aluminium hydroxide, magnesium hydroxide and Camalox in addition contains calcium carbonate. The intragastric consumption of these two antacids was much higher than their respective theoretically available neutralizing capacity (Alucol 3.9 times, Camalox 2.4 times). In-vitro studies demonstrated that interaction with oxo reduced the neutralizing capacity of the two antacids at pH 3.5 from 3.9 mol/l to 1.7 mol/l (Alucol) and 2.5 mol/l (Camalox). This potency loss was related to the aluminium hydroxide content of the two antacids. This study indicates that the neutralizing capacity of antacids is not predictable from their reactivity in aqueous solution and is markedly reduced by protein-containing foods.
Adult↗
Pharmacokinetic interactions with digoxin.
Numerous pharmacological agents have been shown to produce clinically significant pharmacokinetic interactions with digoxin. Drugs which reduce digoxin absorption include the antacids aluminium hydroxide, magnesium hydroxide and magnesium trisilicate, the antidiarrhoeals kaolin and pectin, the hypocholesterolaemic agent cholestyramine and the chemotoxins cyclophosphamide, vincristine and bleomycin. Certain antibiotics including sulphasalazine, neomycin and aminosalicylic acid reduce digoxin absorption while others, including erythromycin and tetracycline, increase the bioavailability of digoxin in some patients. Capsule preparations of digoxin in solution are less subject to several of the interactions which affect the absorption and bioavailability of digoxin tablets. Various drugs induce alterations in the volume of distribution and clearance of digoxin. Cardiac patients receiving digoxin therapy are particularly prone to interactions with commonly co-administered medications such as the antiarrhythmics quinidine and amiodarone, the calcium channel blockers verapamil and nifedipine, and possibly some vasodilating agents. Studies of digoxin interactions have yielded discrepant results, indicating the need for careful analysis of investigational design before arriving at clinical conclusions.
Digoxin↗
Effect of two antacids on the bioavailability of paracetamol.
The effect of two antacids on the bioavailability of paracetamol has been investigated in 12 young healthy volunteers. Following a random cross over design, each subject swallowed, on three separate occasions, one weak apart, 500 mg paracetamol alone, or together with two different aluminium hydroxide, magnesium hydroxide preparations (Dimalan and Maalox). Plasma paracetamol levels were measured by HPLC. The bioavailability of paracetamol was not altered by either antacid, but they both delayed the time to peak plasma concentration (0.85 h; 1.43 h; 1.25 h, without antacid, with Dimalan and with Maalox respectively). The peak plasma concentration was not affected by concurrent antacid administration.
Acetaminophen↗
Nizatidine versus placebo in active benign gastric ulcer disease: an eight-week, multicenter, randomized, double-blind comparison. The Nizatidine Benign Gastric Ulcer Disease Study Group.
STUDY OBJECTIVE: To determine if 150 mg nizatidine twice daily or 300 mg nizatidine at bedtime are similarly effective and to compare each dose with placebo in healing benign gastric ulcers and relieving peptic ulcer symptoms. METHODS: This study was a randomized, double-blind, placebo-controlled parallel comparison. The study was conducted at 74 gastroenterology and internal medicine clinics in the United States and Canada. Four hundred fifty-six patients with active benign gastric ulcer documented by endoscopy participated in the study. On the basis of a computer-generated randomization list, patients were assigned sequentially to receive either 150 mg nizatidine twice daily (n = 151), 300 mg nizatidine once daily at bedtime and identically appearing placebo capsules in the morning (n = 153), or placebo capsules twice daily (n = 152). Treatment lasted for 8 weeks unless healing was documented by endoscopy after 4 weeks. Antacid tablets (aluminum hydroxide, magnesium hydroxide, simethicone combination) were supplied for relief of symptoms. MEASUREMENTS AND MAIN RESULTS: Both doses of nizatidine significantly improved healing rates at 8 weeks compared with placebo. Daytime and nighttime symptom severity was improved by both nizatidine regimens at end point (p less than 0.015 versus placebo, two-tailed test). Antacid use was similar for all groups in the end point analysis. Patient well-being was significantly better in patients treated with nizatidine than in patients in the placebo group ((p less than 0.04, two-tailed test). No clinically significant differences in the incidence of adverse clinical or laboratory events were noted. CONCLUSION: Nizatidine, 300 mg at bedtime and 150 mg twice daily, resulted in greater healing of benign gastric ulcers than placebo treatment after 8 weeks. Relief of the symptoms of gastric ulcer was significantly better in the patients receiving nizatidine treatment versus placebo treatment.
Capsules↗
Effect of antacids on phenytoin bioavailability.
Eight subjects were studied in a randomized crossover design to determine the effect of aluminum-magnesium hydroxide (AMH), calcium carbonate (CC), and aluminum hydroxide-magnesium trisilicate (AHMT) on the bioavailability of a single, 600-mg dose of phenytoin administered orally. Each subject received phenytoin alone on two separate occasions and phenytoin plus each of the three antacids on three other occasions. Each antacid was administered as 160 mEq at 1 and 3 hr after each meal and at bedtime on the day phenytoin was given. The mean area under the curve (AUC) was significantly decreased by AMH (p less than 0.005) and CC (p less than 0.05). AHMT had a similar trend but did not reach statistical significance (p = 0.1). Large inter- and intrasubject variability in AUC was observed when phenytoin was administered alone. In two subjects, cumulative urinary 5-(4-hydroxyphenyl)-5-phenylhydantoin at 72 hr (HPPH72) was determined. The amount of HPPH recovered had similar trends as the AUC with antacid treatments but not the same magnitude. In this study, antacids altered not only the extent of absorption but also appeared to alter the rate of absorption. Antacids administered in a peptic ulcer regimen may decrease the AUC of a single dose of phenytoin. Patients should be cautioned against concomitant use of antacids and phenytoin.
Adult↗
Bioavailability of the oral selective phosphodiesterase 4 inhibitor cilomilast.
STUDY OBJECTIVE: To determine the absolute bioavailability of cilomilast, and assess the effects of food, dosing time, and coadministration of antacid agents on its bioavailability and pharmacokinetics in healthy volunteers. SETTING: Clinical pharmacology unit. DESIGN: Five prospective pharmacokinetic studies: one single-blind, dose-escalating, placebo-controlled trial; four open-label, randomized studies. SUBJECTS: Ninety-six healthy adult volunteers who were nonsmokers. INTERVENTION: In the first study, four subjects received intravenous cilomilast 1, 2, and 4 mg. In the second study, 16 subjects received oral cilomilast 15 mg or intravenous cilomilast 4 mg. In the other three studies, a total of 76 subjects were given single oral 15-mg doses; one study compared its effects in fed versus fasted subjects, one looked for differences of morning versus evening dosing, and one examined coadministration with aluminum hydroxide-magnesium hydroxide. MEASUREMENTS AND MAIN RESULTS: After intravenous administration of cilomilast, plasma concentrations increased in an approximately dose-proportional manner; the half-life, approximately 6.5 hours, was dose independent. Cilomilast clearance and volume of distribution were small. After oral dosing, the absolute bioavailability was consistently close to 100%. Absorption was slower in fed subjects than in fasted (median 2-hr delay in time to reach maximum plasma concentration, average 39% reduction in maximum plasma concentration), but the area under the concentration-time curve from time zero to infinity (systemic availability) was unaffected. Pharmacokinetic parameters were not influenced by time of dosing or coadministration of antacid. CONCLUSION: The absolute bioavailability of oral cilomilast was 100%; it was not adversely affected by time of dosing or coadministration with food or antacid.
3',5'-Cyclic-AMP Phosphodiesterases↗