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At least 307 records · Page 17Linked to original sources
PubMed1992

Adsorption of paracetamol and chloroquine phosphate by some antacids.

The adsorption of paracetamol and chloroquine phosphate onto some antacids with adsorptive properties, has been studied. Dissolution of the drugs from commercial tablets was significantly retarded in the presence of the antacids. The adsorption and retardation of dissolution of both drugs by the adsorbent antacids studied followed the rank order magnesium trisilicate greater than magnesium oxide greater than aluminium hydroxide greater than edible clay. The concomitant administration of the drugs and antacid formulations containing any of these should be discouraged.

Acetaminophen↗
PubMed2001

Antacid increases survival of Vibrio vulnificus and Vibrio vulnificus phage in a gastrointestinal model.

Viable counts of three strains of Vibrio vulnificus and its phage were determined during exposure to a mechanical gastrointestinal model with or without antacid for 9 h at 37 degrees C. V. vulnificus was eliminated (>4-log reduction) within 30 min in the gastric compartment (pH decline from 5.0 to 3.5). Viable V. vulnificus cells delivered from the gastric compartment during the first 30 min of exposure reached 10(6) to 10(8) CFU/ml in the intestinal compartment after 9 h (pH 7.0). Phages were eliminated within 45 min in the gastric compartment (pH decline from 5.1 to 2.5). Less than a 2-log reduction of phage was observed in the intestinal compartment after 9 h (pH 7.0). When the gastric compartment contained antacid V. vulnificus counts decreased slightly (<2 log) during 2 h of exposure (pH decline from 7.7 to 6.0), while counts in the intestinal compartment (pH 7.5) reached 10(7) to 10(9) CFU/ml. Phage numbers decreased 1 log after 2 h in the gastric compartment (pH decline from 7.7 to 5.7) containing antacid and decreased 1 log in the intestinal compartment (pH 7.6) after 9 h. Presence of antacid in the gastric compartment of the model greatly increased the ability of both V. vulnificus and its phage to survive simulated gastrointestinal transit and may be a factor involved with oyster-associated illness.

Animals↗
PubMed2001

Antacid-induced rickets in infancy.

A 3-month-old premature infant presented with a "soft skull." Clinical and radiologic findings confirmed the diagnosis of rickets. Biochemistry revealed normal serum parathyroid hormone (PTH) and undetectable urine phosphate. These findings combined with a history of 5-6 weeks' treatment with high-dose aluminum-rich antacid established the diagnosis of antacid-induced rickets. Discontinuation of the medicine combined with phosphate and vitamin D supplementation resulted in quick resolution of all clinical, radiologic, and biochemical abnormalities. Our patient demonstrates that in premature infants antacid-induced rickets can develop within a few weeks; normal serum PTH concentration and hypophosphaturia are highly indicative of the diagnosis, and contrary to the situation in adults in whom hypercalciuria has been often described, in infants hypocalciuria is more commonly observed. Pediatricians should avoid or minimize the use of aluminum-containing antacids, and when used, carefully monitor mineral metabolism.

Antacids↗
PubMed1980

A comparative crossover study on the treatment of heartburn and epigastric pain: Liquid Gaviscon and a magnesium--aluminium antacid gel.

Forty-four patients with symptoms of gastro-oesophageal reflux were randomly assigned in a crossover trial to treatment for 15-day periods with Liquid Gaviscon (a reflux suppressant) or an antacid gel containing magnesium and aluminium hydroxide. Good relief of symptoms was reported by 84% of patients during therapy with Liquid Gaviscon compared to only 23% during antacid therapy. Relief of symptoms was obtained within 15 minutes by 68% of patients during therapy with Liquid Gaviscon compared to only 9% during antacid treatment. The beneficial effect lasted for more than 4 hours in 75% of patients during treatment with Liquid Gaviscom compared to only 23% of patients obtaining long-term relief during antacid therapy.

Abdomen↗
PubMed1985

Prophylaxis of stress ulcers: antacid titration vs. histamine2-receptor blockade.

The near universal occurrence of stress ulcers in critically ill patients emphasizes the need for early and effective prophylaxis. Intraluminal gastric acidity, ischemic insult to the bowel, and the presence of stress factors are the major precipitants of stress ulcers. The use of H2-receptor antagonists vs. antacid titration for stress ulcer prophylaxis is reviewed. The goals of preventive therapy are to eliminate the stress factors and to maintain intragastric pH greater than 5. Hourly gastric pH monitoring and antacid titration are the mainstay of stress ulcer prophylaxis, with high potency antacids being the preferred agents. H2-receptor antagonists may serve as adjuncts in patients requiring large doses of antacids or having acid-base abnormalities from high gastric output states.

Antacids↗
PubMed2005

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↗
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↗
PubMed1996

Metabolic alkalosis and myoclonus from antacid ingestion.

A patient with a history of cerebrovascular disease, hypertension, and previous gastrectomy developed metabolic alkalosis and myoclonus. His medications included the anti-hypertensive agents nicardipine hydrochloride, delapril, prazosin; dihydroergotoxin and ticlopidine for cerebral infarction; estazolam for insomnia; azuren-L-glutamine compound and S-M powder. In addition, he had taken 12 grams per day of Ohta's Isan antacid, which contained 625 mg sodium bicarbonate per 1.3 g of antacid powder over a 6-month period. This antacid is commonly used in Japan. This is the first report of a case of metabolic alkalosis and myoclonus secondary to ingestion of a commercially available antacid in Japan.

Aged↗
PubMed1986

The ability of antacids and cholestyramine to bind bile acids: effect of pH.

Reflux of bile into the stomach may be injurious to the gastric mucosa. The ability of antacids and cholestyramine to bind bile acids is therefore potentially valuable in the treatment of reflux gastritis. The ability of antacids and cholestyramine to remove bile acids from gastric juice, hepatic bile, and solutions of commercially available bile acids was investigated in vitro over a pH range likely to occur in the stomach. The percentage of bile acids removed by antacids decreased with decreasing initial bile acid concentration and usually decreased as the incubation pH was increased from 3.6 to 7.0. Glycine-conjugated bile acids were bound to a greater extent than taurine-conjugated bile acids and dihydroxy to a greater extent than trihydroxy bile acids. Cholestyramine bound 97-100% of all bile acids in solution at pH 3.6 and pH 7.0. The effect of pH on adsorption should therefore be considered when antacids are used to treat gastritis.

Aluminum Compounds↗
PubMed1986

Antacids and gastric mucosal protection.

Aluminum hydroxide-containing antacids have a protective effect on the stomach in that they prevent grossly visible mucosal necrosis and hemorrhages produced by noxious agents, such as aspirin or absolute ethanol. Histologically, this protective effect is mainly confined to the tissue located deep in the gastric mucosa, essentially comprising gastric glands, while the damage to the surface epithelium is not significantly lessened. Accordingly, integrity parameters of the superficial epithelial layer (potential difference, mucous secretion, cell desquamation) do not indicate a protective action of antacids against damage by necrotizing agents. By contrast, significantly diminished microbleeding rates do suggest that protection by antacids works at a deeper level within the mucosa. The protective action of antacids may be mediated, at least partly, by endogenous prostaglandins, which were found to be elevated in this context.

Animals↗
PubMed1987

Urinary excretion of aluminium after ingestion of sucralfate and an aluminium-containing antacid in man.

Eleven subjects with normal renal function were given, on 2 separate days, at least 1 week apart, four tablets of sucralfate or an aluminium (Al)-containing antacid. The total Al load was approximately 976 mg with the antacid and approximately 828 mg with sucralfate. The daily urinary excretion of Al was measured the day before and during 3 days after drug administration. Al excretion increased significantly after both drugs. There was no significant difference between the two products. The median absorption calculated as percentage of Al dose was 0.005% (range, 0.001-0.017%) for sucralfate and 0.006% (range, 0.002-0.060%) for the antacid. Thus, measurable quantities of aluminium is absorbed after administration of sucralfate, and the drug should, like Al-containing antacids, be given with caution to patients with renal failure.

Adult↗
PubMed1988

Effect of a single dose of antacid on gastric and duodenal bulb pH in duodenal ulcer patients.

Gastric and duodenal bulb pH was measured simultaneously with a multiple pH electrode system in 15 duodenal ulcer patients. A single dose of 10 ml antacid was given 120 min after a liquid standard meal, and the pH was measured for another 90 min. The effect of antacid on duodenal pH, expressed as the time pH is kept above 3.0, was on an average 60 min--shorter in patients with a high gastric acid secretion and longer in normosecretors (p less than 0.01). Regression analysis of simultaneously measured gastric and duodenal bulb pH after antacid showed a highly significant linear correlation with a slope of 1.43, which is significantly greater than 1.0 (p less than 0.01), indicating that antacid has a more pronounced effect on duodenal pH than on gastric pH.

Adult↗
PubMed1988

Treatment with cimetidine, antacid, or placebo in patients with dyspepsia of unknown origin.

Patients with dyspepsia of unknown origin were randomly allocated to a controlled double-blind study to examine the symptomatic effect of cimetidine and antacid especially on the relief of pain, nausea, and bloating. Two hundred and twenty-two patients with no previous history of peptic ulcer disease and no evidence of other organic causes of dyspepsia were treated for 6 weeks with placebo, cimetidine, or antacid. The results showed that cimetidine was superior to both placebo and antacid in relieving pain and nausea but not bloating. Certain background factors, such as epigastric pain and symptoms relieved by solid food, had a significant positive influence on the outcome of treatment. When the impact of background factors was taken into account, cimetidine was found to be more effective than both placebo and antacid also with regard to the number of patients who improved in general well-being.

Adolescent↗
PubMed1989

Symptomatic effect of a low-dose antacid regimen in reflux oesophagitis.

The symptomatic effect of a 2-week low-dose antacid tablet regimen was assessed in a prospective, double-blind, randomized, placebo-controlled, crossover trial in 47 patients with endoscopically verified reflux oesophagitis. During treatment with antacid there were lower global symptomatic scores (p less than 0.05), less acid regurgitation (p less than 0.05), and fewer days (p less than 0.01) and nights (p less than 0.05) with heartburn than during placebo therapy. Also, significantly more patients preferred antacid than placebo treatment (p less than 0.05). Thus, a low-dose antacid tablet regimen relieves symptoms significantly better than placebo in patients with reflux oesophagitis.

Adult↗
PubMed1991

Effect of misoprostol and antacids on gastric and duodenal mucosal enzyme activities in duodenal ulcer patients.

The activities of 11 marker enzymes from the gastric and duodenal mucosa were determined in 15 patients with active duodenal ulcer disease before therapy, after 4 weeks of therapy with the prostaglandin E1 analogue misoprostol, 400 micrograms twice daily, and after another 4 weeks without any therapy. Another 15 patients were given a high-dose liquid antacid regimen. The activities were measured in homogenized material obtained with forceps through an endoscope. The healing rates of the two groups at 4 weeks were 53% and 80%, respectively. No changes in mucosal inflammation were noted during therapy. During treatment with misoprostol the activities in the descending duodenum of the membrane enzymes alkaline phosphatase, leucyl-beta-naphthylamidase, gamma-glutamyltransferase, and 5'-nucleotidase increased towards the values seen in normal controls. Despite a higher healing rate, no changes in the enzyme activities occurred in the group given high-dose antacid therapy. Four weeks after cessation of therapy the enzyme activities in the misoprostol group were not significantly different from the pretreatment values. In the biopsy specimens from the duodenal bulb the activities of monoamine oxidase fell during treatment with misoprostol and were restored to the pretreatment activity when therapy was stopped. In the stomach mucosa the enzyme activities were largely unchanged during treatment with both misoprostol and antacids. These results indicate that misoprostol and antacids have different mechanisms of action but may also suggest that the demonstrated enzymic changes are unrelated to the healing process.

Alprostadil↗
PubMed1994

Nosocomial pneumonia in mechanically ventilated patients receiving antacid, ranitidine, or sucralfate as prophylaxis for stress ulcer. A randomized controlled trial.

OBJECTIVE: To assess three anti-stress ulcer prophylaxis regimens in mechanically ventilated patients for bacterial colonization, early- and late-onset nosocomial pneumonia, and gastrointestinal bleeding. DESIGN: Randomized controlled trial. PATIENTS: Consecutive eligible patients with mechanical ventilation and a nasogastric tube. Of 258 eligible patients, 244 were assessable. SETTING: Medical and surgical intensive care units. INTERVENTION: At intubation, patients were randomly assigned to receive one of the following: antacid (a suspension of aluminum hydroxide and magnesium hydroxide), 20 mL every 2 hours; ranitidine, 150 mg as a continuous intravenous infusion; or sucralfate, 1 g every 4 hours. MEASUREMENTS: Using predetermined criteria, the incidence of gastric bleeding, gastric colonization, early-onset pneumonia, and late-onset pneumonia was assessed in patients intubated for more than 24 hours. RESULTS: Of 244 assessable patients, macroscopic gastric bleeding was observed in 10%, 4%, and 6% of patients assigned to receive sucralfate, antacid, and ranitidine, respectively (P > 0.2). The incidence of early-onset pneumonia was not statistically different among the three treatment groups (P > 0.2). Among the 213 patients observed for more than 4 days, late-onset pneumonia was observed in 5% of the patients who received sucralfate compared with 16% and 21% of the patients who received antacid or ranitidine, respectively (P = 0.022). Mortality was not statistically different among the three treatment groups. Patients who received sucralfate had a lower median gastric pH (P < 0.001) and less frequent gastric colonization compared with the other groups (P = 0.015). Using molecular typing, 84% of the patients with late-onset gram-negative bacillary pneumonia were found to have gastric colonization with the same bacteria before pneumonia developed. CONCLUSION: Stress ulcer prophylaxis with sucralfate reduces the risk for late-onset pneumonia in ventilated patients compared with antacid or ranitidine.

Adult↗
PubMed1998

Pharmacokinetic drug interaction study: administration of ceftibuten concurrently with the antacid mylanta double- strength liquid or with ranitidine.

This study investigated the influence of antacid (Mylanta Double-Strength Liquid; J & J-Merck Consumer, Fort Washington, PA) and the H2 antagonist ranitidine on the pharmacokinetics of ceftibuten, a once-daily oral cephalosporin. Eighteen male volunteers received, in a randomized, three-way, crossover design, a single oral 400-mg dose of ceftibuten after an overnight fast (1) alone, (2) with antacid (60 mL), and (3) with ranitidine (after 3 days of dosing, 150 mg/12 hours). Serial blood and urine samples were collected during a 24-hour period after each administration, with a 1-week washout between treatments. Ceftibuten, and its metabolite ceftibuten-trans, were analyzed in plasma and urine by high-performance liquid chromatography. Bioavailability parameters, maximum plasma concentration and area under the plasma concentration-time curve to infinity of ceftibuten were unaffected by treatment with antacid. These parameters were somewhat higher when ceftibuten was administered with ranitidine, but they were still within the ranges seen in normal healthy volunteers. The excretion of ceftibuten was independent of treatment. The concentrations of ceftibuten-trans were low in both plasma and urine with all three treatments. It is concluded that the co-administration of antacid and ranitidine are unlikely to affect the bioavailability and antibacterial efficacy of ceftibuten.

Administration, Oral↗
PubMed1999

Non-steroidal anti-inflammatory drug gastropathy: clinical results with antacids and sucralfate.

The efficacy of antacids in the short- and long-term treatment of peptic ulcers, has suggested a possible use in the prevention and in the treatment of non-steroidal anti-inflammatory drug related gastroduodenal lesions. In short-term prevention studies, significant protection against ASA-related lesions was observed when antacids at high-dose were given before the administration of the offending drug. To the contrary, antacids at low dose did not prevent ASA-induced lesions of gastric and duodenal mucosa. As for long-term prophylaxis, no clinical effect was observed. In the treatment of non-steroidal anti-inflammatory drug-related mucosal lesions in patients who were able to discontinue the offending drugs, antacids proved of some use, when compared with placebo, but were significantly less effective than H2 blockers, as cimetidine. Sucralfate is an effective antiulcer drug thought to provide cytoprotective action. Although initial studies utilizing sucralfate for protection against short-term aspirin administration were encouraging, longer term studies (more than 7 days) were generally disappointing. A comparative study with misoprostol demonstrated that the PGE1 analogue was far superior for the prevention of non-steroidal anti-inflammatory drugs ulcers, and that ulceration rates in the sucralfate group were equivalent to rates in the placebo group. As far as the treatment of non-steroidal anti-inflammatory drug-related mucosal lesions is concerned, sucralfate proved superior to placebo, similar to ranitidine, but significantly less effective than omeprazole.

Antacids↗