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PubMed1976

Effect of chronic antacid ingestion on serum gastrin and gastric secretion.

Basal gastrin and acid secretion, and histamine- and food-stimulated acid secretion were examined before and after 6 weeks of regular antacid consumption by 20 normal volunteers, in order to test the hypothesis that regular use of antacids produces gastrin cell hyperplasia, altered gastrin inhibition by acid, and gastric hypersecretion. We found no differences in fasting serum gastrin, basal or maximal histamine-stimulated acid, or acid output in response to a protein meal after consumption of commercial antacids with or without calcium carbonate. The results suggest that normal subjects do not acquire functional hyperactivity of the gastrin mechanism after a period of regular antacid use.

Adult↗

PubMed1979

A controlled study comparing cimetidine treatment to an intensive antacid regimen in the therapy of uncomplicated duodenal ulcer.

The authors report the results of a randomized study in which comparison was made between two different kinds of treatment in patients affected by uncomplicated duodenal ulcer endoscopically diagnosed. The first group was treated with 1 g of cimetidine per day, during a period of four weeks (200 mg three times a day and 400 mg at bedtime); the second with a liquid Al-Mg antacid compound, 210 ml/day 30 ml, 1 and 3 hr after meals and 30 ml before bedtime) for four weeks. Fity-one patients were studied, 27 treated with cimetidine, 24 with antacids. At the end of the four-week period, 21 patients (77.7%) in the cimetidine group and 18 patients (75%) in the antacid group were completely healed. Benign side effects were remarked in both types of treatment, none of which made it necessary to suspend treatment. No significant variation of the basal and peak acid output before and after each kind of treatment was observed, while a slight but significant increase in fasting serum gastrin concentration was noted after treatment in the antacid group.

Adult↗

PubMed1977

The action of antacids on serum gastrin concentrations in man.

The effects of two doses of NaCl and NaHCO3 as well as of Al(OH3) and AlCl3 respectively, on serum gastrin concentrations and intragastric pH were compared in duodenal ulcer patients. Also the effect of one dose of an AlPO4 containing commercial antacid on serum gastrin concentration and intragastric pH was studied in duodenal ulcer patients and in a control group. Care was taken to induce swallowing at the times the substances were given through an orogastric tube. The study showed that antacids elicited significantly greater gastrin responses than their non-buffering chloride compounds and that the rise of gastrin after a single dose of antacid was small but significant in duodenal ulcer patients and insignificant in non-ulcer controls. Several factors as rising intragastric pH, individual responsiveness, duodenal ulcer state, vagal influences, the participating ions and their amount contribute to the rise of gastrin after antacids.

Aluminum↗

PubMed1989

Effect of antacid treatment on endogenous prostaglandin synthesis in human antral and duodenal mucosa.

Using 14C-labeled arachidonic acid as precursor for in vitro prostaglandin synthesis, the effect of an antacid containing Al (OH)3, Mg(OH)2 and CaCO3 on endogenous prostaglandin synthesis was investigated in antral and duodenal mucosa of healthy volunteers. After three weeks of treatment with a high-dose antacid, there was no detectable change in the total capacity of the mucosa for prostaglandin synthesis, but the prostaglandin profile was markedly altered. The relative amounts of PGE2 and PGF2 alpha synthesized by antral and duodenal mucosa increased at the expense of the prostaglandins A2/B2, thromboxane A2, and prostacyclin. In a short-term study, this change was not observed following a single antacid dose within 1 hr after application. It is concluded that long-term antacid treatment may alter the prostaglandin pattern formed by gastroduodenal mucosa and this may be related to its therapeutic effect.

Adult↗

PubMed1990

Putative mechanisms of cytoprotective effect of certain antacids and sucralfate.

An investigation of cytoprotective activity of certain antacids and inert particles was carried out by treating ethanol-induced gastric mucosal damage in rats in order to clarify possible mechanisms by which aluminum-containing antacids act. Al(OH)3 inhibited gastric mucosal damage in a dose-related and time-dependent manner. Neither aluminum ions themselves nor the particle size of the Al(OH)3 complex were responsible for the observed cytoprotection, since neither AlCl3, chemically inert Al2O3*C, nor sea sand showed protective effects. Hyperosmolality in the gastric lumen was not a deciding factor in inducing cytoprotection. Silicic acid and titanium dioxide, with superficial charge similar to Al(OH)3 proved to be effective in inhibiting gastric hemorrhagic lesions and releasing PGE2, suggesting that the surface charge of Al(OH)3 may be important in its cytoprotective properties. The same may also be valid for sucralfate. Since antacid-induced cytoprotection was only partly reduced by pretreatment with indomethacin, it is likely that additional mechanisms and mediators other than prostaglandins, such as nonprotein sulfhydryls, also are involved in gastric cytoprotection arising from aluminum-containing antacids.

Aluminum Hydroxide↗

PubMedDate not supplied

Is upper gastrointestinal radiography necessary in the initial management of uncomplicated dyspepsia? A randomized controlled trial comparing empiric antacid therapy plus patient reassurance with traditional care.

STUDY OBJECTIVE: To compare two strategies for the evaluation and management of patients who have had acute dyspepsia for four days or more: empiric high-dose antacid therapy combined with patient reassurance (empiric care) versus therapy based on prompt upper gastrointestinal radiography (traditional care). DESIGN: Prospective, randomized trial. The patients in the empiric care group were reassured that upper gastrointestinal radiography was not necessary and were subsequently treated with high-dose empiric antacid therapy (15-30 ml of high-potency antacid one and three hours after meals and at bedtime). The traditional care group after meals and at bedtime). The traditional care group received upper gastrointestinal radiography as part of the initial evaluation. Subsequent treatment was determined by individual physicians based on test results. SETTINGS: Fee-for-service, hospital-based primary care practice and Veteran's Administration medical center outpatient clinic. PATIENTS: All patients were less than 70 years of age and without gastrointestinal bleeding, anemia, significant weight loss, or other specified symptoms of severe acid peptic disease. Fifty patients were randomized to traditional care, and 51 to empiric care. Pre-randomization clinical features were identical with the exception of sex distribution and baseline disability. MEASUREMENTS AND MAIN RESULTS: After six months of follow-up, there were no significant differences in symptom scores, disability, satisfaction, and quality of life measures (as measured by the Sickness Impact Profile scores) between the two groups. Findings were unchanged when adjusted for sex, study site, alcohol consumption, and cigarette smoking. Of the radiographs obtained in the traditional care group, 13 (27%) showed duodenal ulcer disease, gastritis, or duodenitis. There were no serious complications of ulcer disease or therapy noted in either group. The average costs per patient associated with traditional care at one study site were greater, $286 versus $116 (p less than 0.0001). CONCLUSIONS: Select patients with dyspepsia receiving a combination of reassurance and empiric antacid therapy do as well as patients whose initial management strategy includes upper gastrointestinal radiography, at a substantially lower cost.

Adult↗

PubMedDate not supplied

Empiric antacids and reassurance for acute dyspepsia.

The evaluation of ambulatory patients with dyspepsia frequently includes upper gastrointestinal radiographs (UGIs), a practice of unproven value in low-risk patients. To assess an alternative management strategy without UGIs, 28 patients with upper abdominal pain seen in an adult medical walk-in practice were treated with high-dose antacid therapy for three weeks. The clinical course on antacid therapy was good; 68% of patients reported substantial improvement. Initial requests for UGIs were high among both patients and physicians. Following empiric antacid therapy, requests for UGIs fell from 68% to 32% for patients (p = 0.05) and from 71% to 21% for physicians (p = 0.001). No serious complications were detected after 18 months of follow up. Direct medical charges were reduced by 37%. Empiric antacid therapy for patients at low risk for serious disease relieves dyspepsia and reduces both patient and physician requests for UGIs.

Adult↗

PubMedDate not supplied

A comparative bioavailability study to estimate the influence of an antacid on droxicam pharmacokinetics.

The influence of an antacid on droxicam pharmacokinetics was investigated in 12 healthy male volunteers. A two way cross-over study was performed after the oral administration of 20 mg of droxicam (Ombolan capsules) and droxicam together with an antacid (Mucal powder). The plasma concentrations of piroxicam, the active moiety of droxicam, were determined by a high-performance liquid chromatographic method. The pharmacokinetic parameter values (mean +/- RSD) of piroxicam after administration of droxicam alone were: AUC0-->infinity = 125.5 +/- 25.1 micrograms.h/l, Cmax = 2.08 +/- 19.9 micrograms/l, tmax = 7.08 +/- 36.8 h and t1/2 = 46.3 +/- 27.0 h. Following administration of droxicam together with the antacid the values obtained for the same parameters were: AUC0-->infinity = 135.1 +/- 24.1 micrograms.h/l. Cmax = 1.85 +/- 23.9 micrograms/l, tmax = 8.17 +/- 34.9 h and t1/2 = 52.0 +/- 22.4 h. These results indicate that concurrent administration of the antacid does not significantly change the bioavailability and pharmacokinetics of droxicam.

Administration, Oral↗

PubMed1981

Cimetidine and antacid prophylaxis of acute upper gastrointestinal bleeding in high risk patients. Controlled, randomized trial.

A randomized, controlled clinical trial was performed to compare the efficacy of prophylactic cimetidine treatment, antacid treatment and no treatment in high risk patients. Sixty patients received cimetidine (200 mg every 6 hours), 52 patients received antacids (Maalox, 10 ml/hour), and 56 patients received no treatment. One hundred thirty-five patients completed the study. Eight patients in the control group and one patient in the antacid-treated group presented with upper gastrointestinal bleeding. No bleeding occurred in the cimetidine-treated group. Patients considered at low risk had no bleeding. Cimetidine or antacid prophylaxis significantly decreased the incidence of upper gastrointestinal bleeding in the high risk patients.

Antacids↗

PubMed1986

Healing of benign gastric ulcer with low-dose antacids and fiber diet.

A randomized, double-blind, placebo-controlled trial was conducted to determine the efficacy of a low-dose aluminum-magnesium antacid regimen (Link one tablet q.i.d.) (total neutralizing capacity 120 mmol HCl/day) in combination with a high- or a low-fiber diet in ulcer healing and relief of symptoms in patients with benign gastric ulcer. After 6 wk, the ulcer healed in 28 (67%) of the 42 patients treated with antacids compared with 11 (25%) of the 44 patients treated with placebo (p less than 0.001). Antacids were also significantly more effective than placebo in the relief of symptoms. The dietary treatment did not significantly influence ulcer healing or ulcer symptoms. Constipation was more frequently seen with the low- than with the high-fiber diet (p less than 0.01). No significant side effects from antacids were recorded.

Adult↗

PubMed1986

Antiulcer effect of rioprostil, a prostaglandin E1 analog, in combination with antacid.

Rioprostil, a primary alcohol prostaglandin E1 analog, is currently undergoing clinical evaluation for use in the treatment of peptic ulcer disease. Since antacids are often used in conjunction with other antiulcer agents, studies were conducted to determine if concomitantly administered antacid modifies the antiulcer activity of rioprostil. This investigation showed that concomitant administration of antacid (0.25-1.0 ml Maalox) does not inhibit the ability of rioprostil (0.125-4.0 micrograms/kg, p.o.) to prevent ethanol-induced gastric lesions in rats. The antiulcer effect of the drug combination was additive, suggesting that each compound acts independently to prevent gastric bleeding. These results in animals suggest that clinically the use of antacid will not compromise the efficacy of rioprostil and that the combination may be a useful mode of therapy for the treatment of peptic ulcer disease.

Alprostadil↗

PubMed2004

Pharmacokinetics and relative bioavailability of clofazimine in relation to food, orange juice and antacid.

BACKGROUND: Clofazimine is potentially useful for the treatment of disease due to multidrug resistant Mycobacterium tuberculosis, as well as leprosy and certain chronic skin diseases. Its pharmacokinetics have been incompletely characterized. This study was conducted to explore issues relating to bioavailability in the presence of food, orange juice, and antacid. METHODS: A 5 drug regimen consisting of clofazimine, cycloserine, ethionamide, para-aminosalicyclic acid, and pyridoxime was administered to healthy subjects four times using a four period cross-over design with two weeks washout between treatments. Subjects also received orange juice, a high fat meal, aluminum/magnesium antacid, or only water in random order with the drug regimen. The pharmacokinetics of clofazimine were assessed using individual- and population-based methods and relative bioavailability compared to fasting administration was determined. RESULTS: Clofazimine exhibited a sometimes prolonged and variable lag-time and considerable variability in plasma concentrations. From the population analysis (one-compartment model), the mean oral clearance was 76.7 l/h (CV=74.2%) and mean apparent volume of distribution was 1470 l (CV=36.3%). The first-order absorption rate constant ranged from 0.716 to 1.33 h(-1) (pooled CV=61.7%). Residual (proportional) error was 49.1%. Estimates of bioavailability compared to fasting administration were 145% (90% CI, 107-183%) for administration with high fat food, 82.0% (63.2-101%) for administration with orange juice, and 78.5% (55.1-102%) for administration with antacid. CONCLUSION: Administration of clofazimine with a high fat meal provides the greatest bioavailability, however, bioavailability is associated with high inter- and intra-subject variability. Both orange juice and aluminum-magnesium antacid produced a reduction in mean bioavailability of clofazimine.

Administration, Oral↗

PubMed1988

Antacids reduce Campylobacter pylori colonization without healing the gastritis in patients with nonulcer dyspepsia and erosive prepyloric changes.

Antral biopsy specimens from 89 consecutive patients with nonulcer dyspepsia and erosive prepyloric changes included in a prospective, randomized, double-blind 4-wk study of the effect of an aluminum-magnesium antacid (120 mmol/day) or pirenzepine (50 mg b.i.d.) vs. placebo were examined histologically. Campylobacter pylori (CP) was found by light microscopy of silver-stained sections in 25 patients (28%). Campylobacter pylori-positive patients were on average older than CP-negative patients (p = 0.02). There was a strong association between CP colonization and acute inflammation (p less than 0.001), both being rare in the absence of chronic inflammation. During treatment with antacids, the density of CP decreased (p less than 0.001) without any improvement of the inflammatory reaction. On the contrary, the number of patients with gastritis tended to increase after antacids as compared with placebo (p less than 0.10). A separate analysis showed no symptomatic effect of the drugs. Thus, neither nonulcer dyspepsia nor erosive prepyloric changes are strongly associated with antral CP colonization or acute inflammation. Aluminum-magnesium antacids may suppress antral CP infection without healing the gastritis or relieving symptoms.

Adult↗

PubMed1988

Low-dose antacids or cimetidine for duodenal ulcer?

In a double-blind, randomized, multicenter trial 150 consecutive outpatients with endoscopically verified duodenal ulcer were treated with either a low-dose antacid regimen (1 tablet q.i.d.; acid-neutralizing capacity, 120 mmol/day), or cimetidine (800 mg nocte). After 4 wk of treatment control gastroscopy showed ulcer healing in 54 of 76 patients (71.1%) in the antacid group, as compared with 58 of 74 patients (78.4%) in the cimetidine-treated group. The difference in healing rate of 7.3% (95% confidence interval, -6.5% to +21.1%) was not statistically significant. The symptomatic effect, measured as number of days and nights with ulcer pain, was also quite similar in the two treatment groups. However, the number of days with pain was significantly lower in the first week of treatment in the antacid group (p less than 0.01). Thus, the efficacy of a low-dose antacid tablet regimen approximated that of cimetidine (800 mg nocte) in the treatment of duodenal ulcer patients.

Antacids↗

PubMed1996

Determination of norfloxacin by fluorescence in the presence of different antacids: quantification of analytical interferences.

Norfloxacin is a fluorquinolone that can interfere with certain antacids (derivatives of Al and Mg) because its dissolution profiles are dependent on pH. Furthermore, it can form insoluble complexes that modify its absorption and bioavailability. Two sensitive and selective analytical methods using fluorescence (FL) and UV spectrophotometry (UV) have been developed to study the dissolution behaviour in gastric juice of different formulations of norfloxacin in tablets. There are no significant differences when the samples are measured by both methods and their ruggedness in the presence of some excipients is proven. From this, it is concluded that they are effective for this study. When different antacids are added to the dissolution medium, using UV and FL methods with the same samples, totally different dissolution profiles appear. Using FL, it would appear that up to 400% of the amount of norfloxacin in the tablet is released. These profiles are misleading because the uniformity of dosage units was tested before the dissolution studies. It is proven that the antacids dissolved in gastric juice do not produce fluorescence, but cause important analytical interferences with norfloxacin. This may be because their association with Al3+ or Mg2+ forms a new compound. Nevertheless, it is observed that this effect is more important in some antacids (Almagate, Magaldrate). This may be because their ability to deliver Al to the medium is greater.

Aluminum Hydroxide↗

PubMed1998

Altered pharmacokinetics of halofantrine by an antacid, magnesium carbonate.

This study investigated the in vitro adsorption of halofantrine (Hf) by some antacids. Magnesium carbonate showed the highest adsorptive effect, the extent of adsorption being up to 83%. Only 4% of Hf adsorbed by the antacid could be eluted with 0.1 M HCl while no detectable elution occurred with water. Other antacids investigated were magnesium trisilicate and aluminium hydroxide and these had Hf-adsorption capacities of 23 and 43%, respectively. The effect of magnesium carbonate on the bioavailability of Hf was evaluated in seven healthy volunteers. The subjects were administered with 500 mg oral dose of Hf-HCl or the same dose of the drug in combination with 1 g of magnesium carbonate, in a crossover fashion. Blood samples were collected at predetermined time intervals and were analysed for Hf and its major metabolite, desbutylhalofantrine (Hfm), using high-performance liquid chromatography method. The results showed that magnesium carbonate significantly prolonged (P<0.05) the time to reach maximum plasma concentration (Tmax) of Hf. Also the maximum plasma concentrations (Cmax) of Hf and Hfm were significantly reduced (P<0.05). Furthermore, there was a reduction in the area under the curve (AUC) values of Hf and this was as high as 56% (range 1-56%). Results of this study suggest that it may not be advisable to concomitantly administer Hf with an antacid like magnesium carbonate.

Adsorption↗

PubMed1993

Characterization of antacid compounds containing both aluminum and magnesium. I. Crystalline powders.

The composition and antacid properties of 10 samples of crystalline antacids containing both aluminum and magnesium were determined. The composition was found to vary significantly, even within the same type of antacid. For example, three of four hydrotalcite samples exhibit evidence of the presence of a minor phase of amorphous aluminum hydroxide. Almagate and almagcit, which are claimed to be unique compounds, were found to be composed of hydrotalcite, magnesium hydroxycarbonate, and/or magnesium carbonate and amorphous aluminum hydroxide. All three magaldrate samples examined contained a minor phase of amorphous aluminum hydroxide. All 10 samples passed the preliminary antacid test and had high acid neutralizing capacities. However, the rate of acid neutralization varied between samples. In some cases the rate of acid neutralization at a dose of 400 mg was too slow to raise the pH to 3.0 as required by the Rossett-Rice test.

Aluminum↗

PubMed1998

[Phosphate deficiency as a rare cause of osteomalacia--case report of several years of enteral feeding and antacid therapy].

HISTORY AND CLINICAL FINDINGS: Floor-of-the-mouth cancer had been diagnosed and surgically treated in a 55-year-old man 4 years before the latest admission. For the last 3 years he had been fed through a percutaneous endoscopic gastrostomy (PEG). Since then he had experienced reflux oesophagitis which was being treated with aluminium-containing antacids. He was hospitalized for the surgical treatment of bilateral fractures of the neck of the femur. A surgical biopsy revealed osteomalacia but no metastasis. INVESTIGATIONS: The serum phosphate level was significantly reduced (0.21 mmol/l) and there was no detectable phosphate excretion in the 24-hour urine. Serum calcium concentration was unremarkable, but there was hypercalciuria (34.4 mmol/d). Alkaline phosphate activity was significantly raised (393 U/l) and parathormone level reduced (7 ng/l). Vitamin D concentration was unremarkable. TREATMENT AND COURSE: The phosphate content in the parenteral feed was at first increased and additional phosphate was given by mouth. The calcium and phosphate levels slowly became normal only after medication had been changed from antacids to H2-blockers. CONCLUSIONS: In this case osteomalacia was caused not by vitamin D deficiency but by a lack of phosphate. The reduced intestinal phosphate absorption by the antacids only partially explains the pronounced clinical signs. If antacids are taken over long periods the phosphate balance should be carefully monitored to avoid osteomalacia.

Alkaline Phosphatase↗