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At least 217 records · Page 12Linked to original sources
PubMed2006

Clinical and laboratory studies of the antacid and raft-forming properties of Rennie alginate suspension.

BACKGROUND: Acid pockets at the gastro-oesophageal junction escape buffering from meals in the stomach. Combining high-dose antacid with alginate may therefore be of benefit in gastro-oesophageal reflux disease. AIM: To characterize the antacid and raft-forming properties of Rennie alginate suspension (containing high-dose antacid and alginate; Bayer Consumer Care, Bladel, the Netherlands). METHODS: The in vitro acid-neutralizing capacity of Rennie algniate was compared with Gaviscon (Reckitt Benckiser, Slough, UK) by pH-recorded HCl titration. Alginate raft weight formed in vitro at different pH was used to evaluate the pH dependency of raft formation with each product. A double-blind, placebo-controlled, randomized crossover study also compared the antacid activity of Rennie alginate vs. placebo in vivo using continuous intragastric pH monitoring in 12 healthy fasting volunteers. RESULTS: Compared with Gaviscon, Rennie alginate had a higher acid-neutralizing capacity, greater maximum pH and longer duration of antacid activity in vitro. However, the two products produced comparable alginate rafts at each pH evaluated. In vivo, Rennie alginate provided rapid, effective and long-lasting acid neutralization, with an onset of action of <5 min, and duration of action of almost 90 min. CONCLUSIONS: The dual mode of action of Rennie alginate offers an effective treatment option for mild symptomatic gastro-oesophageal reflux disease particularly considering recent findings regarding 'acid pockets'.

Adolescent↗
PubMed1979

Concurrent administration of antacids and prednisone: effect on serum levels of prednisolone.

1 Specific radioimmunoassays have been developed for the measurement of prednisolone and prednisone in serum. 2 Serum prednisolone levels have been measured following the administration of prednisone both with and without antacids. 3 There were no significant differences in the values of Cmax (mean +/- s.d.) (251 +/- 80 ng/ml with, 245 +/- 69 ng/ml without antacid), AUC (1430 +/- 469 ng ml-1 h-1 with, 1406 +/- 530 ng ml-1 h-1 without antacid) or Tmax (1.6 +/- 0.6 h with, 1.6 +/- 0.8 h without antacid). 4 Serum prednisone levels were less than 20% of prednisolone levels at all time intervals in the subjects studied. 5 Concurrent antacid administration has no significant effect on serum prednisolone levels attained.

Antacids↗
PubMed2005

Reduced oral itraconazole bioavailability by antacid suspension.

AIMS: To investigate the effects of antacid suspension on oral absorption of itraconazole. METHODS: A randomized, open-labelled, two-period, crossover study with a 1-week washout period was conducted in 12 healthy Thai male volunteers. The participants were allocated in either treatment A or B in the first period. In treatment A, the volunteers were orally administered with 200 mg of itraconazole alone. In treatment B, the volunteers were administered orally with 200 mg of itraconazole co-administered with antacid suspension. Serial serum samples were collected over the period of 24 h and subsequently analysed by using a validated high-pressure liquid chromatographic method with ultraviolet detection. Pharmacokinetic parameters were determined by non-compartmental analysis. RESULTS: Time to reach maximal concentration (Tmax), maximal concentration (Cmax) and area under the curve (AUC0-infinity) were markedly decreased in antacid-treated group. Tmax for treatment A was 3.0 +/- 0.4 and 5.1 +/- 2.7 h for treatment B. Cmax and AUC0-infinity of treatments A and B were 146.3 +/- 70.5 vs. 43.6 +/- 16.9 (ng/mL) and 1928.5 +/- 1114.6 vs. 654.8 +/- 452.2 (ng x h/mL) respectively. 90% Confidence interval (90% CI) of Cmax and AUC0--infinity were 24.1-42.1 and 16.2-65.9 respectively. CONCLUSIONS: Rate and extent of itraconazole oral absorption were markedly decreased by concurrent use of antacid suspension. Hence, co-administration of itraconazole and antacid suspension should be avoided.

Adolescent↗
PubMed1990

Antacid-induced phosphate depletion syndrome presenting as nephrolithiasis.

A 29-year-old insulin-dependent diabetic woman developed phosphate depletion, nephrolithiasis and bilateral ureteric obstruction due to antacid abuse. Unlike previous descriptions of chronic phosphate depletion, myalgia, weakness and bone pain were absent. Biochemical features included hypophosphataemia, hypercalciuria, hypophosphaturia, elevated plasma, 1,25-dihydroxyvitamin D and low plasma intact parathyroid hormone. These abnormalities were corrected when antacid ingestion was reduced and phosphate intake supplemented. We propose that phosphate depletion secondary to antacid abuse caused 1 alpha-hydroxylase activation and elevation of the plasma 1,25-dihydroxyvitamin D level, leading to marked hypercalciuria. Once diagnosed, antacid abuse is a readily reversible cause of hypercalciuria and renal stones. Moreover, antacid-induced phosphate depletion may present with nephrolithiasis in the absence of musculoskeletal symptoms. This report is intended to draw attention to this important cause of renal stone disease.

Adult↗
PubMed1990

The effect of an antacid and food on the absorption of cimetidine and ranitidine.

The effect of varying doses of a liquid antacid preparation containing magnesium hydroxide, aluminum hydroxide and simethicone on the absorption of the H2-receptor antagonists, cimetidine and ranitidine, was determined in 2 groups of 11 volunteers; one group fasted and one group fed a standardized breakfast. The antacid alone caused a significant decrease in the AUC of cimetidine (24%). Similarly, concomitant antacid caused a 59% decrease in the AUC of ranitidine. There were no effects on any of the other pharmacokinetic parameters examined. The absorption of both drugs was similar in fasted and fed volunteers, but in the fed volunteers the antacid did not produce the decrease in AUC seen in the fasted volunteers. These data suggest that H2-receptor antagonists should not be taken at the same time as antacids.

Adolescent↗
PubMed1989

Inhibition of enoxacin absorption by antacids or ranitidine.

Ten normal volunteers participated in a randomized, five-way crossover study to determine the effect of concurrent enoxacin and antacid or ranitidine administration on enoxacin absorption. The bioavailability of a single oral 400-mg enoxacin dose was significantly decreased, by 73 and 49%, when Maalox TC was administered 0.5 and 2 h before enoxacin, respectively. Enoxacin bioavailability was not significantly altered when the antacid was given 8 h before or 2 h after enoxacin administration. Ranitidine, administered intravenously 2 h before enoxacin, also significantly decreased enoxacin bioavailability, by 40%. The correlation between the proximity of antacid administration and the magnitude of the decrease in enoxacin bioavailability supports complexation as the mechanism of the antacid-enoxacin interaction. However, reduction of enoxacin bioavailability by ranitidine suggests that elevated gastric pH may also play a role in the antacid-enoxacin drug-drug interaction.

Adolescent↗
PubMed1990

Inhibition of norfloxacin absorption by antacids.

The effect of antacids on the systemic absorption of oral norfloxacin was evaluated in 12 healthy volunteers. Subjects were given each treatment in a balanced sequence at 7-day intervals. Treatments included 400 mg of norfloxacin alone, 400 mg of norfloxacin 5 min after aluminum-magnesium hydroxide (Maalox), Maalox 2 h after 400 mg of norfloxacin, and 400 mg of norfloxacin 5 min after calcium carbonate (Titralac). Blood and urine samples were collected at predetermined time intervals for 24 and 48 h, respectively. Norfloxacin concentrations in plasma and urine were determined by high-pressure liquid chromatography. The area under the plasma concentration-versus-time curve from time zero to infinity and urinary recovery were used to compare the relative bioavailability of norfloxacin with antacids with that of norfloxacin alone. Norfloxacin bioavailability was markedly reduced when subjects received antacid pretreatment. When norfloxacin was given 5 min after Maalox and Titralac, the bioavailabilities were 9.02 and 37.5%, respectively, relative to that for 400 mg of norfloxacin alone. When Maalox was given 2 h after norfloxacin, maximal concentrations of norfloxacin in plasma occurred between 1 and 1.5 h postdose, and absorption was reduced to a lesser extent, with a relative bioavailability of 81.31%. Norfloxacin concentrations in urine were also reduced as a result of antacid administration. Antacids containing aluminum and magnesium salts and calcium carbonate should be avoided by patients taking norfloxacin.

Absorption↗
PubMed2004

Pharmacokinetics of posaconazole coadministered with antacid in fasting or nonfasting healthy men.

Posaconazole is a potent broad-spectrum azole antifungal agent in clinical development for the treatment of invasive fungal infections. This study evaluated the potential for a pH-dependent pharmacokinetic interaction between posaconazole and an antacid (Mylanta), under fasting and nonfasting conditions. Twelve men completed this randomized, four-period crossover, single-dose study. Subjects received 200 mg of posaconazole following a 10-h fast, with 20 ml of Mylanta and a 10-h fast, with 20 ml of Mylanta and a high-fat breakfast, and with a high-fat breakfast alone. Antacid coadministration had no statistically significant effects on posaconazole bioavailability under fasting or nonfasting conditions. In the fasting state, antacid slightly increased the relative oral bioavailability of posaconazole by 15% (P = 0.296); in the nonfasting state, antacid decreased the relative bioavailability of posaconazole by 12% (P = 0.352). Food increased the relative oral bioavailability of posaconazole by 400% (P = 0.001). In conclusion, the effect of antacid on posaconazole exposure in the fasting or nonfasting state was small and is not considered clinically significant.

Adolescent↗
PubMedDate not supplied

Effect of antacid and ascorbic acid on serum salicylate concentration.

To determine the effect of antacid or ascorbic acid administration on plateau serum salicylate concentrations, nine healthy subjects were given each of the following treatments by balanced block design: choline salicylate (equivalent to 3.76 or 5.62 Gm/day of aspirin); choline salicylate plus magnesium-aluminum hydroxide (120 ml/day); or choline salicylate plus ascorbic acid (3 Gm/day). In subjects developing a control serum salicylate level above 10 mg/dl, antacid administration produced a decrease in serum salicylate level (mean 19.8 mg/dl vs. 15.8 mg/dl) (P less than 0.01). Ascorbic acid administration was not associated with a significant change in serum salicylate. The reduction in serum salicylate following antacid appears to be due to antacid-induced alkalinization of the urine with resultant increase in renal salicylate clearance. Antacid administration should be considered a potential cause of altered serum salicylate concentration in patients receiving large doses of salicylate.

Adult↗
PubMed1994

In vitro buffering capacities of proprietary non-particulate antacids available in New Zealand.

Four commercially available non-particulate antacid preparations were titrated against 1M hydrochloric acid to assess buffering capacity as compared to 30 ml 0.3M sodium citrate solution. All antacids were used in the manufacturers "unit dose". All antacids tested demonstrated some in vitro buffering capacity, and "Eno" (Reckitt and Colman) had a buffering capacity similar to that of sodium citrate. The retail cost per unit dose was established for each proprietary antacid and for sodium citrate. It was concluded that while proprietary antacids are cheaper per dose than sodium citrate, preparations differ in their acid-neutralising capacity.

Antacids↗
PubMedDate not supplied

Drug-antacid interactions: assessment of clinical importance.

Antacids and adsorbents are commonly used preparations that are generally considered to be pharmacologically inert and free from adverse effects. They may, however, interact with a diverse range of primary drugs and the sequelae can be disadvantageous to the efficacy of the primary medication. Many such reports in the literature are based on animal experiments, or on single-dose studies in healthy subjects. Some reports are anecdotal and are unconfirmed; others are based solely on in vitro evidence. Potentially important interactions have been suggested for a relatively small group of drugs: tetracyclines, phenytoin, digoxin, chloroquine, cimetidine, quinidine, nonsteroidal antiinflammatory drugs, and beta-blocking agents. The evidence for these has been critically evaluated, as well as for antacid-anticoagulant and antacid-nitrofurantoin interactions that have been wrongly emphasized in the literature. The majority of literature reports on interactions with antacids have been overemphasized; only ferrous sulfate-, isoniazid-, and tetracycline-antacid interactions fall into a category I importance (scale I-III of descending importance). This category is for those interactions with good evidence of actual or potential importance in patients or in relevant studies on normal subjects.

Adrenergic beta-Antagonists↗
PubMed2003

Metabolic bone disease after chronic antacid administration in an infant.

OBJECTIVE: To describe a case of hypophosphatemia and metabolic bone disease (MBD) due to aluminum-containing antacids. CASE SUMMARY: An 8-month-old white boy was brought to the emergency department due to irritability and pain with movement. Upon examination, the infant was irritable, unable to bear weight, had palpable clavicular bony lesions, point tenderness of the hips, and poor head control. The infant had lost several developmental milestones over the past 4 months (eg, ability to roll over) and had decreased appetite and minimal weight gain. Skeletal survey revealed multiple rib fractures, osteoporosis, and Ricketts. Hypophosphatemia (2.3 mg/dL; normal 3.2-6.3) and an elevated serum aluminum level (14 microg/L, normal 0-9) were noted. Past medical history was positive for gastroesophageal reflux. He had been started on ranitidine and aluminum hydroxide (1/2 teaspoonful per 6-ounce bottle) at 2 months of age. The infant's formula contained elevated aluminum levels. Further investigation showed that 1/2 tablespoonful instead of 1/2 teaspoonful of antacid had been added to each 6-ounce formula bottle for the prior 6 months; only 1 month of antacid therapy had been recommended. An objective causality assessment revealed a probable adverse drug event. DISCUSSION: Phosphate-binding substances such as aluminum-containing antacids can bind large amounts of phosphorus, causing hypophosphatemia and MBD. CONCLUSIONS: We report this case to increase awareness of the risk of hypophosphatemia and MBD (likely aluminum related) with use of over-the-counter aluminum-containing antacids in pediatrics, as well as the hazards of prescribing doses in "spoonful" units.

Aluminum Hydroxide↗
PubMed1994

Drug interactions with antacids. Mechanisms and clinical significance.

Concomitant use of antacid preparations with other medications is common. The potential for antacid-drug interactions is dependent upon the chemistry and physical properties of the antacid preparation. The intragastric release of free aluminum and magnesium ions has potent effects on gastrointestinal function and on drug pharmacokinetics. Antacid-drug interactions may occur secondary to changes in gastrointestinal motility or alterations in gastric and urinary pH. Direct adsorption also results in decreased drug bioavailability. Human drug interaction studies are usually performed with healthy volunteers; extrapolation of these results to clinical situations may not always be valid. However, the current literature would suggest that significant interactions with antacids do occur with certain members of the quinolone, nonsteroidal anti-inflammatory drug (NSAID) and cephalosporin classes of drugs. Notable interactions also occur with tetracycline, quinidine, ketoconazole and oral glucocorticoids. These interactions are particularly relevant in the patient with sepsis, cardiac disease or inflammatory syndromes.

Administration, Oral↗
PubMed1992

Effect of antacid medication on the pharmacokinetics of temafloxacin.

The effect of an antacid drug (Maalox 70) on the pharmacokinetics of temafloxacin was studied in 12 healthy young volunteers. The study was designed as a randomised open 2-period crossover trial in which temafloxacin was administered alone and with Maalox 70. In both treatments, temafloxacin was administered as a single oral 400mg dose on the morning of day 2. In the antacid regimen, 8 doses of Maalox 70 were administered every 2h on day 1, starting at 8am and ending with the last dose at 10pm; 5 doses were given on day 2, at 2.5 and 1h before administration of temafloxacin and 1, 3 and 5h after the temafloxacin dose. With coadministration of Maalox 70, peak plasma temafloxacin concentrations (Cmax) were reduced to 44.6% (+/- 24.5), and AUC(0-infinity) was reduced to 39.8% (+/- 17.4) of the corresponding values obtained when temafloxacin was given alone. Urinary excretion of temafloxacin was reduced to 46.0% (+/- 13.7) of that observed when temafloxacin was administered alone. Time to peak plasma concentration (tmax = 1.8h) was not affected by antacid administration. Comparable or greater antacid-associated reductions in relative bioavailability have been reported for other quinolones. As with other quinolones, the concurrent administration of temafloxacin and antacids should be avoided.

Adult↗
PubMed1982

Controlled clinical trial of duodenal ulcer healing with antacid tablets.

The effect of an antacid tablet regimen (total acid-neutralizing capacity, 280 mmol/day) and placebo was studied in 75 patients with duodenal ulcer in a double-blind 4-week trial. The ulcer healed in 30 out of 37 (81%) patients treated with antacids as compared with 9 out of 38 (24%) patients treated with placebo (p less than 0.001). Ulcer symptoms in the antacid- and the placebo-treated groups did not differ significantly until the last week of treatment (p less than 0.01). Both constipation and diarrhoea were slightly more common in antacid- than in placebo-treated patients (NS). Serum concentration of aluminium increased significantly (p = 0.01), whereas serum concentrations of calcium, phosphorus, magnesium, iron, and total iron-binding capacity did not change during treatment. No other side effects of antacids were recorded. Thirty-eight patients with unhealed ulcer after cessation of the antacid/placebo treatment were treated openly with 150 mg ranitidine twice daily. The ulcer healed in 31 out of 37 (83%) patients (one drop-out) after 4 weeks' treatment, and only one patient remained with unhealed ulcer after 6 weeks' ranitidine treatment. No side effects due to ranitidine were recorded.

Adult↗
PubMed1985

Duodenal ulcer healing with four antacid tablets daily.

In a double-blind, randomized, multicenter trial in 80 consecutive outpatients with endoscopically verified duodenal ulcer, we have tested the ulcer-healing efficacy of a quite low dose of antacids, given only four times daily. The patients received one chewable aluminum-magnesium-antacid tablet (buffering capacity, 30 mmol/tablet) or placebo 1 h after meals and at bedtime. Re-endoscopy after 4 weeks of treatment showed healed ulcer in 28 of 38 patients (74%) in the antacid group, compared with 11 of 38 patients (29%) in the placebo group (p less than 0.001). The number of days and nights with ulcer pain was significantly less in the antacid group than in the placebo group during the treatment period. Thus, only four antacid tablets a day, with a total buffering capacity of 120 mmol/day, significantly promote duodenal ulcer healing and pain relief.

Adult↗
PubMed1987

Gastric prostaglandin E2 release induced by aluminium hydroxide and aluminium hydroxide-containing antacids in rats. Effect of low doses and citric acid.

Suspensions of aluminium hydroxide or a commercial antacid containing aluminium hydroxide (Trigastril) was instilled intragastrically in rats in doses comparable to high and low human therapeutic doses (aluminium hydroxide, 125 mg and 12.5 mg/kg, respectively). Corresponding experiments were carried out with 0.6% citric acid added to the antacid suspensions. Prostaglandin E2 (PGE2) in the gastric content was analysed by radioimmunoassay 6 h after drug administration. Both high and low doses of aluminium hydroxide and Trigastril increased the concentration of PGE2 significantly. Citric acid did not significantly affect the antacid-induced PGE2 release except in combination with a low dose of aluminium hydroxide, with which a significant increase was seen. Release of PGE2 by low doses of antacids implies the possibility that enhanced cytoprotection may be involved in the mechanism by which antacids promote the healing of peptic ulcers.

Aluminum Hydroxide↗
PubMed1990

Maintenance of duodenal ulcer healing by antacids.

Three studies have investigated the ability of long-term antacid treatment to prevent duodenal ulcer relapse. The first of these, more than 30 years ago, showed that antacids could reduce recurrence or persistence of symptoms when compared with placebo. There are two studies from the 'modern era' of fibreoptic endoscopy and H2-reception antagonists. The Milan study found antacid (one tablet four times daily), cimetidine (400 mg at night), or a combination of the two, to be approximately equally effective in the prevention of relapse. The international study found antacid (three tablets three times daily) to be as effective as cimetidine (400 mg at night) and to be better than placebo for maintenance purposes. Antacid, three tablets at night had intermediate efficacy.

Antacids↗