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PubMed1988

Influence of prolonged antacid administration on rat gastric mucosa.

The effect of long-term administration of an antacid preparation on the gastric mucosa was investigated in rats, special attention was directed towards hypergastrinaemia and density of argyrophil cells. One ml of an Al (OH)3- and Mg (OH)2-containing antacid (in vitro neutralization capacity 28 mmol/die) or water was administered intragastrically 4 times daily. An additional group of rats remained untreated. Twelve hours after the final dose serum gastrin levels were significantly (p less than 0.001) elevated (113 +/- 28 pg/ml) compared to the control groups (33 +/- 1 and 22 +/- 2 pg/ml). Antral gastrin (G)-cell density was also increased after antacids by 58% whereas the somatostatin (D)-cell density and the somatostatin concentration in antral tissues were decreased. The number of fundic D- and argyrophil cells were not altered by antacid treatment. The number of parietal cell declined significantly in response to antacids. The foveolar gland region was almost doubled after antacids. It is concluded that in the rat 1. despite persistent hypergastrinaemia due to chronic antacid administration increases in argyrophil cell densities are not to be found; 2. long-term administration of antacids exert a trophic effect on the corpus mucosa predominantly by an increase of mucus neck cells.

Aluminum Hydroxide↗
PubMed1978

Cimetidine, antacid, and hospitalization in the treatment of benign gastric ulcer: a multicenter double blind study.

Two hundred forty patients with benign gastric ulcer were treated in a controlled clinical trial to assess the effect on healing of cimetidine, antacids, and hospitalization. Inpatients and and outpatients were randomly assigned to one of three treatments: cimetidine plus antacid, cimetidine plus dummy antacid, or placebo tablet plus antacid. In 206 patients who met criteria for analysis, ulcer healing as shown by endoscopy occurred by 12 days in 11 to 26 percent and by 42 days in 58 to 76 percent. There were no significant differences in healing between hospitalized and nonhospitalized patients or between treatment subgroups. Symptomatic response was equivalent in all groups. The median antacid consumption was 328 mEq of in vitro buffering capacity per day. Patients taking antacids experienced significant diarrhea compared with those taking no antacid. This investigation suggests that the effect of cimetidine is equivalent to that of large amounts of antacid, but because a true placebo group was not studied it is not possible to conclude from this study alone whether either agent influenced healing. In contrast to widespread belief, initiation of treatment in the hospital did not enhance healing, but because patients were not randomly assigned to inpatient and outpatient status no final conclusion about the effect of hospitalization on healing can be drawn.

Adult↗
PubMed1979

Treatment of duodenal ulcer with antacid and sulpiride. A double-blind controlled study.

The effect of aluminum-magnesium hydroxide tablets (800 mg seven times per day) and that of sulpiride, a hypothalamic neurolaptic, were studied in 101 patients with duodenal ulcer in a double-blind controlled 4-wk trial. Significantly more of the patients treated with antacid, sulpiride, or antacid-sulpiride combination showed a greater than 50% reduction in ulcer size than did the patients treated with placebo. However, only in the antacid- and antacid-sulpiride-treated groups did the ulcer, with and without residual inflammation, disappear statistically more often than in the placebo-treated group. Furthermore, only in the antacid-sulpiride-treated group did complete healing, with no trace of inflammation, occur statistically more often than in the placebo-treated group. Disappearance of ulcer pain was likewise statistically more frequent in the antacid-sulpiride group than in the placebo-treated group. Antacid therapy with aluminum-magnesium hydroxide tablets appears to accelerate the rate of ulcer healing. Sulpiride appears to have a minor but definite synergism with antacids. Cigarette smoking affected ulcer healing adversely; on the other hand, factors favorable to healing were the early onset age of ulcer symptoms and acid hypersecretion. Male patients also healed more favorably than females.

Administration, Oral↗
PubMed1984

[The effect of 4 different antacids on the gastrointestinal tract and mineral metabolism].

In a double-blind, randomized study, six healthy women were given four different antacids containing aluminium, magnesium or calcium, for a period of seven days, respectively. The antacids investigated were Trigastril 50 Del, Maaloxan Suspension, Kompensan-S forte Suspension and Solugastril 50 Gel. All the antacids tested led to a significant increase in the stool frequency and accelerated stool transit time. The sodium-containing agent produced a significantly greater acceleration as compared with the other antacids. No changes in the sodium, potassium or calcium blood levels were seen prior to and after administration of the various antacids. All preparations reduced phosphate concentrations (significant only with Solugastril an Trigastril). In the case of Maaloxan with a high content of magnesium, the magnesium concentration was increased mildly, but significantly. Irrespective of the dose of aluminium employed, all the antacids resulted in a significant increase in aluminium concentration of between 23 and 36 micrograms/l. All the antacids significantly reduced the excretion of phosphate in the urine. The preparation with a high level of magnesium produced the greatest excretion of magnesium, the preparation containing calcium the greatest excretion of calcium, in 24-hour urine. The results show that the effects on the weight of the stools, the transit time, the consistency of the stools, and on the mineral balance, depends upon the composition of the respective antacid.

Aluminum↗
PubMed1984

Functional cytoprotection by certain antacids.

The effect of different antacids has been investigated on ulcer development, parameters of mucus barrier disruption and gastric PGE2 content in rats. Al(OH)3-containing antacids inhibit gastric ulcer formation induced by alcohol or acetylsalicylic acid (ASA). Changes in parameters of mucus barrier disruption evoked by sodium taurocholate can be significantly diminished by treatment with antacids. This protective effect of antacids is abolished in animals pretreated with indomethacin. PGE2 contents both in gastric mucosa and instillate are increased by pretreatment with antacids. PGE2 content in gastric mucosa or instillate diminished by sodium taurocholate can be normalized by antacid treatment. Although acidic isotonic or acidic hypertonic solutions increase gastric PGE2 content, they are not ulceroprotective. In these solutions, detectable amounts of released PGE2 are minimal. Under in vitro circumstances, the lifetime of PGE2 in gastric juice is shortened by decreasing pH. It has been concluded that Al(OH)3-containing antacids increase PGE2 content in the gastric mucosa. Furthermore, they are capable of lengthening the lifetime of PGE2 in the gastric content. Thus, the clinical use of Al(OH)3-containing antacids in low doses is to be emphasized in the management of gastric ulcer disease.

Animals↗
PubMed1982

In vitro evaluation of liquid antacid products.

The in vitro neutralizing capacities, sodium content, and cost of 21 nonprescription antacid products were compared. A 5-ml sample of each antacid product was placed in a beaker using a pipette. The pipette was rinsed three times wtih purified water 5 ml, and the mixture was stirred with a magnetic stirring rod. After one minute, 1.0 N hydrochloride acid 30 ml was added to the mixture and stirring was continued for 15 minutes. The pH was then measured. Using a burette, sufficient 0.5 N sodium hydroxide was added to the mixture to raise the pH stable value to 3.5. Samples were tested in duplicate. Manufacturers were requested to provide sodium content for the antacid products, and costs were obtained based on wholesale prices. Neutralizing capacity of the antacids ranged from 1.3 to 8.7 meq/ml. Of the 21 products, 17 contained at least 90% of the claimed neutralizing capacity, as required by FDA. One product did not qualify as an antacid by FDA standards. Sodium content has been reduced in may preparations and may no longer be a factor in choosing an antacid. Chronic therapy with antacids can be expensive, and it costs more to deliver a given amount of neutralizing capacity with less concentrated antacids.

Antacids↗
PubMed1998

Are antacids necessary as routine prescriptives with non-steroidal anti-inflammatory drugs?

In Singapore, there exists a local habit to routinely prescribe antacids with non-steroidal anti-inflammatory drugs (NSAIDs) perhaps in the belief that gastrointestinal (GI) symptoms and complications are common, and that antacids protect from them. We prospectively studied 140 adults in an orthopaedic clinic who were prescribed a short course of NSAIDs (1 to 4 weeks) without antacids to determine the frequency and severity of GI symptoms. Symptomatic patients were then given antacids to determine their effect on the GI symptoms and followed up by telephone interview. These patients had mild inflammation, soft tissue rheumatism, injury or degenerative disease. All were otherwise well with no known peptic ulcer disease or major illness and were not on ulcerogenic drugs. Only 13 (9.3%) had significant GI symptoms, of which 6 (4.2%) of the total took antacid and 5 (3.5%) had partial or total relief. In this study, GI symptoms were not common with short course NSAIDs in otherwise well patients. Antacids may afford symptomatic relief for GI symptoms. However, because antacids may offer no significant protection against NSAID-induced peptic ulcer, may dangerously mask symptoms of GI irritation, may be troublesome to take and costly on a large scale, we should stop routine prescription of antacids in patients requiring only short-term NSAIDs and not at risk for peptic ulcer disease.

Adolescent↗
PubMed1995

Comparative Effects of Liquid Antacids on Esophageal and Gastric pH in Patients with Heartburn.

This double-blind crossover trial compared the postmeal effects of single doses of liquid antacids on esophageal and gastric pH in patients with a history of heartburn. Treatment consisted of one of two antacids containing the same active components---aluminum and magnesium hydroxide---but different in vitro acid-neutralizing capacities (ANCs). The pH was assessed continually from 1 h before a refluxogenic meal to 4 h after its completion in 24 subjects who received 20 ml of Mylanta((R)) Double Strength (MYL-20: ANC = 101.6 mEq), 20 or 30 ml of Extra-Strength Maalox((R)) Plus (MA-20, MA-30: ANC = 116.2 and 174.3 mEq, respectively), or placebo (ANC = 0) in random order. Esophageal pH increased rapidly and significantly (p < 0.05) to peak values of 7.0--7.4 with antacid. The increase in mean esophageal pH values was significantly higher (p < 0.05) than placebo for 30 min with MA-20 and for at least 70 min with MYL-20 and MA-30. In contrast, gastric pH rose slowly to mean peaks of 2.9--3.1 with antacid. During this interval, only MYL-20 was associated with significant improvements (p < 0.05 versus placebo) in total number of reflux episodes and total time that esophageal pH measured >4. Thus, ANC alone is not a useful guide in predicting in vivo antacid behavior, as in this study where the antacid dose with the lowest ANC demonstrated a duration of action as long or longer than that of antacid doses with higher ANC values. The rapid, prolonged increases in esophageal pH that preceded modest changes in gastric pH strongly suggest that the lower esophagus is the primary site of antacid action for heartburn relief.

Journal Article↗
PubMed1984

Controlled therapeutic trial to determine the optimum dose of antacids in duodenal ulcer.

Antacids are widely used in the management of duodenal ulcer but the optimum dose of antacid required for ulcer healing has not been determined. We therefore studied 107 patients with endoscopically diagnosed duodenal ulcer who were allotted at random to one of the following treatment groups; placebo (group P) and antacid (groups A, B and C). A liquid antacid (Aludrox MH, Wyeth) with neutralising capacity of 2.3 mmol HCl/ml was administered in graded doses of 7.5 ml (Group A), 15 ml (Group B), and 30 ml (Group C), one hour and three hours after each meal, six times a day for four weeks. Patients in group P received 15 ml liquid placebo in a similar fashion. Complete symptomatic relief was obtained in 33% of patients in the placebo group, 54% in antacid group A, 89% in group B, and 92% in group C. Endoscopic assessment at the end of four weeks of treatment gave an ulcer healing rate of 29% in the placebo group, 46% in group A (103.5 mmol antacid/day), 85% in group B (207 mmol/day), and 88% in group C (414 mmol/day). There was no significant difference in the healing rates and pain relief between placebo and antacid group A, while both groups B and C had significantly higher ulcer healing rates and pain relief compared with placebo (p less than 0.001) and antacid group A (p less than 0.01). Drug related unwanted effects were recorded only in group C - 28% of patients suffered from diarrhoea. It is concluded that the optimum antacid requirements for the treatment of duodenal ulcer is 90 ml (acid neutralising capacity, 207 mmol HCl) per day.

Adult↗
PubMed1987

Phosphate-binding properties and electrolyte content of aluminum hydroxide antacids.

The phosphate-binding capacities of 19 liquid and solid aluminum hydroxide gel antacids were determined in vitro under varying pH conditions. The resulting data provide a basis explaining the phosphate-binding characteristics observed when patients are treated with long-term aluminum hydroxide therapy. No antacid, liquid or solid, showed significant binding at pH 1.0. Maximum phosphate binding (expressed as phosphorus; P) was observed at pH 2.0 and 3.0 for most antacids and decreased markedly at alkaline pH. The liquid antacids showed a significantly greater phosphate-binding capacity than did tablets or capsules (p less than 0.01). At pH 2.0, the liquid antacids bound a mean of 22.3 mg P/5 ml. At pH 8.0 binding was reduced to a mean of 7.3 mg P/5 ml. Significant interbrand differences were observed. At pH 2.0, the solid antacids bound a mean of 15.3 mg P/tablet or capsule. At pH 8.0, binding was reduced to a mean of 5.8 mg P/tablet or capsule. Interbrand differences, while substantial, were less than those observed among the liquid antacids. Variations in sodium and potassium content were clinically insignificant for most of the antacids in this study, while the differences in phosphate-binding properties were sufficient to warrant attention in the patient with renal failure.

Aluminum Hydroxide↗
PubMed1986

Antacids for peptic ulcer: do we have anything better?

During recent years several reports have appeared documenting that antacids containing aluminium hydroxide accelerate the healing process of duodenal ulcer. In gastric ulcer, however, only one study has demonstrated an effect clearly superior to that of placebo. Several studies, in both gastric and duodenal ulcer patients, have not been able to demonstrate any significant difference between antacids and H2 blockers with respect to ulcer healing and symptom relief. An important acknowledgement is the fact that the doses of antacids required for ulcer healing are much smaller than first assumed, and that tablet formulations of antacids are at least as effective as liquid antacid suspensions. The excellent effect of the more convenient low-dose tablet regimens has strengthened the position of antacids in the competition with other anti-ulcer drugs. Usually, side effects of low-dose antacid regimens are few and mild. In patients with impaired renal function, accumulation of absorbed aluminium may have serious consequences. However, in patients with healthy kidneys, aluminium is quickly excreted after absorption, and unhealthy effects are not documented. Antacids should therefore still constitute a cornerstone in the treatment of peptic ulcers.

Adult↗
PubMed1992

[In vivo and vitro study of prostaglandins E2 and I2 participation in protective function of antacids on gastric mucosa].

Antacids apart from neutralization of hydrochloric acid possess the gastro-protective properties. In this paper, performed in vivo and in vitro, we studied the effects of antacids (aluminium and magnesium hydroxides) on secretion of PGE2 and 6-keto-PGF1 alpha (a stable metabolite of PGI2) by the gastric mucosa and isolated gastric mucosal cells of rats. We studied protective effects of these drugs on the gastric mucosa and isolated cells as well. It was shown that antacids stimulate generation of PGE2 and PGI2 in the gastric mucosa and protect it against alcohol-induced damage. Indomethacin given prior to antacids in a dose (1 mg/kg) which did not cause any gastric mucosal changes but inhibited generation of both prostaglandins, abolished protective effects of antacids. In comparison with control, surface epithelial cells of the gastric mucosa isolated from the stomachs of rats which were treated with antacids earlier, secreted significantly more PGE2 and PGI2, and were less damaged after incubation with 8% alcohol. Indomethacin inhibited secretion of prostaglandins by isolated surface epithelial cells of the gastric mucosa and abolished protective effects of antacids on these cells. The study confirms both in vivo and in vitro the protective properties of antacids and shows that prostaglandins participate in their action.

Aluminum Hydroxide↗
PubMed1982

Antacid therapy of duodenal ulcer. Effects of smaller doses.

In a previous study, antacids in a dose consuming 480 mmol of acid per day were administered in combination with small doses of trimipramine or cimetidine. The healing rate of duodenal ulcer after 6 weeks' treatment was 85%. In a subsequent study, the dose of antacids was reduced further and antacid tablets were given instead of liquid antacids. In this study, antacids were given alone and the daily dose consumed only 280 mmol of acid. The healing rate of duodenal ulcer after 4 weeks' treatment was 81%, but the symptomatic effect was weak. The effect of this dose of antacid tablets on intragastric postprandial pH was much less than the effect of a therapeutic dose of ranitidine. The high efficacy of smaller doses of antacids on ulcer healing, in spite of a weak effect on acidity, suggests the possibility that, in duodenal ulcer, antacids may act via other mechanisms than neutralization of hydrochloric acid.

Aluminum Hydroxide↗
PubMed1983

Antacid use in an ambulatory elderly population. A report from Dunedin Program.

Antacid use was studied in a population of 3192 elderly ambulatory subjects. Antacids were used by 18.6% of women and 12.9% of men. Three common antacid products accounted for 63.8% of all antacids used by these subjects. Serum phosphorus concentrations of participants using aluminum antacids were significantly lower than in a nonantacid user control group (P less than 0.02). Total protein and serum calcium concentrations of subjects using aluminum and magnesium combination antacid products were significantly lower than the control group (P less than 0.001 and P less than 0.04). Men using calcium carbonate antacids reported diarrhea significantly more frequently than control subjects.

Age Factors↗
PubMed1990

Fate of antacid gel in the stomach. Site of action and interaction with food.

The site of action of a high-power Al-Mg antacid gel (buffering capacity 70 meq/10 ml) and its interaction with food was examined in 10 healthy volunteers. Combined pH-metries in antrum and corpus were performed in each volunteer on four occasions. In a randomized study design, antacid or placebo were given 1 hr after either a protein or a carbohydrate pancake, of which only the former had any acid-buffering capacity. Before the meal, pH was higher in the antrum than in the corpus (median antrum: 3.2, corpus 1.5). In the corpus, a protein pancake but not a carbohydrate pancake raised the pH (median pH after protein pancake: 3.5; after carbohydrate pancake: 1.4). In the antrum, the protein pancake had no effect, but the carbohydrate pancake decreased the pH (median pH after protein pancake: 3.1; after carbohydrate pancake: 2.0). The antacid had no effect in the corpus after either pancake. It raised intraluminal pH markedly in the antrum after a carbohydrate pancake (median antral pH before antacid: 2.0; after antacid: 3.3), whereas its effect in the antrum was weak after a protein pancake. In vitro experiments were conducted to explain the in vivo results: in contrast to a carbohydrate pancake, a protein pancake reduced the buffering capacity of the antacid by direct interaction. In conclusion, the effect of an antacid gel on intragastric pH is predominantly localized in the antrum and is attenuated in the presence of proteins.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Influence of antacid administrations on aspirin absorption in patients with chronic renal failure on maintenance hemodialysis.

In order to investigate the possible interaction between oral aspirin and antacids in uremic patients on chronic hemodialysis, we administered to 5 uremic patients: (1) aspirin alone; (2) aluminum-magnesium hydroxide with aspirin; (3) aluminum-magnesium hydroxide followed (two hours) by aspirin; (4) calcium carbonate simultaneously with aspirin; and (5) calcium carbonate followed (two hours) by aspirin. In all the occasions, aspirin was given two hours after a standard lunch. Both antacid preparations induced comparable changes in aspirin mean peak plasma concentration (Cmax), if given simultaneously with aspirin, whereas no difference was found in other pharmacokinetic parameters. When antacids were followed (two hours) by aspirin, both Cmax and time of maximum concentration (Tmax) were significantly altered in respect to the value with aspirin alone. No changes in the time course of post aspirin serum thromboxane B2 were detected when aspirin and antacids were administered simultaneously, but the inhibition of serum thromboxane B2 was delayed when antacids were followed (two hours) by aspirin. These results indicate that the administration of antacids to uremic patients interferes with absorption of oral aspirin. This interference can be minimized if aspirin and antacids are given simultaneously.

Absorption↗
PubMed2003

The GI Cocktail is no more effective than plain liquid antacid: a randomized, double blind clinical trial.

The "GI Cocktail" is a mixture of medications often given in the Emergency Department (ED) for dyspepsia symptoms. Several combinations are used, but the most effective has not yet been determined. This study compared three combinations commonly given for dyspepsia. The study was a prospective, randomized, double-blinded trial comparing antacid (group 1); antacid + Donnatal (group 2); antacid + Donnatal + viscous lidocaine (group 3) for acute treatment of dyspepsia in the ED. Patients were randomly assigned to receive one of the three medication combinations. Patients rated their discomfort on a Visual Analog Scale (VAS) immediately before receiving the medication and 30 min later. Change in VAS was the primary study endpoint. A 13-mm difference in VAS was considered clinically significant. VAS change in the three groups was compared using multivariable regression, controlling for pretreatment VAS, study drug, previous antacid use, and gastrointestinal (GI) history. One hundred twenty patients were enrolled between July and December 2000. One hundred thirteen subjects (113) completed the protocol: Group 1 (N = 38); Group 2 (N = 37); Group 3 (N = 38). There was no statistically significant difference between the groups in terms of age, gender, GI history, previous antacid use, or initial degree of pain. Group 1 had a 25 +/- 27 mm mean (+/- SD), decrease in pain; Group 2, 23 +/- 22 mm decrease; and Group 3, 24 +/- 26 mm decrease. There was no statistically significant difference in pain relief between the three groups on univariate analysis or multivariable regression. In conclusion, the addition of Donnatal or Donnatal + lidocaine to an antacid did not relieve dyspepsia better than plain antacid. The "GI Cocktail" concoction may not be necessary.

Adult↗
PubMed1988

Antacids: the past, the present, and the future.

Antacids have served us well for over a century. The attitude in the late 1950s to 1970s that antacids should be taken only on demand was unjustified and was based on what can be seen nowadays as misinterpretation of scientific data. Twelve recent endoscopic controlled studies have confirmed the efficacy of antacids in the healing of duodenal ulcer, achieving about 75% healing in 4 weeks. Like H2-receptor antagonists, the efficacy of antacids in the healing of gastric ulcers is controversial, most probably related to the even greater pathogenetic heterogeneity of this condition. Antacids should be given at least four times a day and at least 1 hour after meals, since their therapeutic success most likely depends on neutralization of postprandial acid secretion. In vivo, the newer tablet forms are indistinguishable from the liquid forms in terms of neutralizing efficiency and healing efficacy. The ideal dose is one that neutralizes 400 mmol of acid. Combination with an anticholinergic drug is effective and a recent report suggests that this may lead to longer remission than with H2-receptor antagonists. As a long-term therapy, antacids appear to work but need to be taken in multiple daily doses, a regimen which is unlikely to meet with long-term patient compliance. The success of antacids in duodenal ulcer healing should alert us to the importance of controlling the meal-stimulated acid secretion in ulcer therapy, and to the hard fact that acid is a non-permissive factor in ulcer healing.

Antacids↗