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[The effect of antacids on stress-induced lesions of the gastric mucosa in the piglet (author's transl)].

After administration of antacids, gastric stress lesions due to hemorrhagic shock appear in the pig stomach quicker and more markedly than in animals which have been similarly treated with an indifferent substance or not at all. However, once treated, the administration of antacids seems to favor the healing of mucosal lesions after the end of the stress. At the same time it was observed that after administration of antacids in hemorrhagic shock, the serum gastrin level rises and does not remain constant, as in the control group. An attempt is made to explain the favorable effect of antacids on the genesis of hemorrhagic stress lesions in the pig's stomach through this observation.

Animals↗

[Preoperative administration of antacids to prevent Mendelson's syndrome in pregnant women receiving general anesthesia (author's transl)].

Preoperative administration of 15 mls of the antacid Andursil to women undergoing surgical procedures in GA during pregnancy does reduce the risk of aspiration pneumonitis (Mendelson-Syndrome) from 1:3,5 to 1:15,5. The data show that the number of risk patients is increased in early stages of pregnancy and--surprisingly--in patients undergoing elective surgery. Pains and costs of prophylactic antacids are negligible. Neonates of LSCS patients receiving an antacid are not at an increased risk. As a conclusion the prophylactic administration of oral antacids to all pregnant women having a GA is recommended.

Anesthesia, General↗

In vitro adsorption of some corticosteroids on antacids.

The adsorption of prednisone, prednisolone, fluprednisolone, betamethasone, triamcinolone, beta-methylprednisone acetate and hydrocortisone acetate on various antacids or adsorbents was studied at 37 degrees C. The antacids or adsorbents used were magnesium trisilicate, aluminum hydroxide, bismuth oxycarbonate, magnesium oxide, magnesium carbonate, calcium carbonate, talc, kaolin and charcoal. Magnesium trisilicate and charcoal had the highest adsorption capacity for the corticosteroids tested. Bismuth oxycarbonate and talc had intermediate adsorption properties while kaolin and aluminium hydroxide had lower effects. Other antacids were without any adsorption character. Results of the elution study confirmed the higher affinity of magnesium trisilicate over that of bismuth oxycarbonate and talc for the steroids tested. Further in vivo testings are still needed to assess the effect of antacids on the bioavailability of coadministered corticosteroids.

Adrenal Cortex Hormones↗

Effect of antacid and H2-receptor blocker treatment on gastric endocrine cells.

It has been previously suggested that antral pH governs the density of antral G- and D-cells. Therefore, we investigated the effect of acid neutralization by an antacid (magaldrat; in vivo neutralization capacity of 144 mval/day) and the effect of suppression of gastric acid secretion by an H2-receptor blocker (oxmetidine, 400 mg/day) on the density of both cell types in healthy volunteers and duodenal ulcer patients. Four weeks after antacid treatment antral G-cell density decreased significantly in both groups, while antral D-cells decreased only in volunteers. Basal serum gastrin was not altered, whereas the integrated postprandial serum gastrin response and antral gastrin concentration was significantly reduced in volunteers but not in ulcer patients. None of the parameters investigated was changed by oxmetidine treatment. Considering the short-lasting effect on acid neutralization induced by the antacid dosage used in this study and the inability of oxmetidine treatment to influence volume densities and secretory activities of antral G- and D-cells it is concluded that mechanisms other than a change of antral pH may account for the results obtained during antacid treatment.

Adult↗

[The effect pf antacids on the tissue histamine and prostaglandin (PGE2) content of the gastric mucosa].

Stimulation tests (pentagastrin) induced significant changes in tissue histamine levels in the gastric mucosa within 30 minutes. Acid secretion and a decrease of histamine after application of antacids containing calcium could not be observed in our study; neither was application of antacids over a period of eight days followed by a change in gastric mucosal tissue histamine concentrations. Patients under non-steroidal antiphlogistic medication showed diminished histamine levels. Administration of antacids did not produce changes in histamine levels, but induced a rise of PGE2 levels in the fundal and corpus area of the stomach. This may be due to a cytoprotective effect of antacids containing calcium on the gastric mucosa.

Adult↗

Antacid therapy--changes in mineral metabolism.

Antacid ingestion may lead to side-effects related to their chemical composition. Aluminum hydroxide may cause the phosphate depletion syndrome even during short-term administration of high doses in patients at high risk, such as alcoholics. Long-term intake may lead to bone demineralization and to osteomalacia. Fluoride complexing in the gut and prevention of fluoride absorption may be an additional factor. The clinical relevance of aluminum absorption in patients with normal renal function is not clear. In contrast, in patients with renal failure, aluminum hydroxide ingestion may contribute to an increasing hyperaluminemia. Hyperaluminemia and tissue deposition of aluminum in these patients may contribute to the dialysis-associated encephalopathy. Magnesium hydroxide causes an alkalinization of the urine due to magnesium absorption and urinary excretion. Thus, in renal insufficiency, a life-threatening hypermagnesemia may develop if magnesium-aluminum-containing antacids are prescribed. The milk-alkali syndrome, rarely observed nowadays, may be caused by calcium carbonate- and sodium bicarbonate-containing antacids. Hypercalciuria and alkaluria predispose to nephrolithiasis. The possibility that these disturbances in mineral metabolism will develop in patients with normal renal function is unlikely unless there is an abuse of these "over the counter" antacids.

Aluminum Hydroxide↗

Ranitidine, cimetidine and antacids in the prevention of recurrence after healed duodenal ulcer: one-year experience.

A total of 110 subjects with duodenal ulcer healed with cimetidine (C) (50 patients), ranitidine (R) (40 patients) or pirenzepine (20 patients) was randomly divided in 3 groups. The first group (40 patients) was treated with R (150 mg nightly); the second group (40 patients) with C (400 mg nightly) and the third group with antacids as needed for symptomatic relief. The presence of the ulcer and its healing were established by endoscopy, which was repeated after 6 and 12 months of treatment, or previously if symptoms suggested recurrence. At the end of the year's follow-up, no recurrence of ulcers was observed in 75% of the R group, in 77.5% of the C group and in 40% of the antacids group. Some erosive duodenitis developed in the first and second groups (17.5% and 20% respectively), but none in the antacids group. Most of the ulcers that recurred did so in the first 6 months of treatment. No relevant side-effects were observed with the treatments described. Although no significant difference was detected between C and R treatments, both appeared to be clearly more effective than antacids. The usefulness of adequate prophylactic treatment against the tendency of duodenal ulcer to recur is stressed.

Antacids↗

[Therapy of reflux esophagitis with antacids].

At present it has not been sufficiently established by controlled trials that antacids are more efficacious in the treatment of reflux symptoms and reflux esophagitis than placebo. Furthermore, Gaviscon does not seem to offer advantages in comparison to traditional antacids. It is suggested that the value of antacids in the treatment of reflux esophagitis should be further evaluated in controlled studies using higher antacid dosages for more extended periods of time, at least 8 to 12 weeks.

Antacids↗

[Intragastric pH increase using antacids or secretin for stress ulcer prevention in surgical risk patients].

The efficacy of an antacid or synthetic secretion on elevations in intragastral pH above 4 was tested in a controlled prospective study. 21 surgical high risk patients received an antacid, and 17 secretin. Antacid prophylaxis resulted in a significantly higher intragastral pH than with secretin. This was especially true in patients with several risk factors. The percentage of secretin patients with a pH reduction below 4 was higher. An increase in dosage was necessary in 4 of the 17 patients receiving secretin and in none of those receiving antacids. One stress ulcer hemorrhage occurred during secretin infusion.

Aged↗

Impairment of captopril bioavailability by concomitant food and antacid intake.

Single oral doses of captopril (50 mg) were given in a randomized cross-over study to 10 healthy volunteers after fasting, after a standardized breakfast (440 kcal; 1804 kJ) or with 50 ml of an antacid suspension. Blood and urine samples were analyzed by gas chromatography. The peak captopril concentrations attained were 701 +/- 81 ng/ml (mean +/- s.e.m.) after fasting, 351 +/- 56 ng/ml with an antacid (p less than 0.05) and 140 +/- 14 ng/ml after a meal (p less than 0.01). The peak concentrations were reached in 0.5, 0.9 and 1.5 h (p less than 0.01), and the areas under the blood concentration-time curves were 782 +/- 86, 456 +/- 60 (p less than 0.05) and 344 +/- 47 ng X h/ml (p less than 0.01), respectively. The relative bioavailability of captopril was 0.66 and 0.48 with antacid and after food, respectively. The deleterious effect of food - but not that of antacid - was reflected as a delayed hypotensive activity of captopril.

Adult↗

[Therapy of acute hemorrhage - the value of antacids].

In contrast to prospective studies demonstrating the efficacy of antacids in the prevention of stress ulcers there are only a few reports on the successful treatment of bleeding lesions with antacids. Although by a constant pH exceeding 5.4 acid-induced dissolution of thrombocyte aggregation can be avoided, the high amounts of antacids cause volume problems and side effects. No experience exists on the combination of formula diets with antacids in the treatment of acute hemorrhage.

Acute Disease↗

[Effect of various therapeutic schedules of antacids on the pH of gastric contents in patients with duodenal ulcer].

Ten patients with uncomplicated duodenal ulcer were given three different therapeutic regimens of antacid experiments II, III and IV, and a control regimen, without antacid, named experiment I. Experiment I consisted of a normal diet with three meals a day; experiment II, III and IV consisted of a diet as in experiment I plus 132,06 mEq, 265,92 mEq or 396,88 mEq respectively of antacid divided in six equal doses given one and three hours after breakfast, lunch and dinner. Having been carefully instructed, the patients were intubated with a gastric tube, which was kept in for five days, receiving in each day one of the aforementioned regimens, in a sequential order. The fifth day was reserved for the augmented Histalog test. Each hour from 8 a.m. to 10 p.m., in the first four days, a sample of the gastric juice was aspirated for pH measurement. The statistical evaluation of the acidity of the samples at different times showed that experiment III (265,92 mEq antacid/day) was able to keep the pH over 3 for longer periods of time when compared with experiments I and II and not different from experiment IV. The present investigation emphasize the necessity of clinical trials comparing therapeutic regimens of antacid with different neutralizing capacity, in order to find the most effective dose in the treatment of duodenal ulcer.

Adult↗

Studies on the in vitro interaction of D-penicillamine with antacids.

Interactions of D-penicillamine with various antacids (aluminum hydroxide-magnesium hydroxide, AH-MH; aluminum hydroxide-calcium carbonate, AH-CC; dihydroxy sodium aluminum carbonate, DSAC; aluminum hydroxide, AH) were studied in vitro. Only a small binding to AH-MH (29.2 +/- 7.2 mumol/g antacid) and AH (13.6 +/- 4.0 mumol/g antacid) and no adsorption at all to AH-CC and DSAC were observed. Bile salts and bicarbonate as well as the pH did not influence binding. Although extrapolations from in vitro studies to in vivo conditions are hazardous, clinically relevant interactions of D-penicillamine with antacids in patients ingesting both drugs in the usual dose range simultaneously appear unlikely.

Adsorption↗

Acid-neutralizing capacity and sodium content of antacid products from Belgium.

The acid-neutralizing capacity and sodium content of nine antacid products available in Belgium were evaluated and compared with typical values for Mylanta-II. Liquid and tablets of Mylanta-II have a higher acid-neutralizing capacity per unit dose than do all the other Belgian antacids tested. On a unit dose basis, the sodium contents of the Mylanta-II products are lower than those of all other Belgian antacids tested except Maalox products. Because the minimum recommended dose (MRD) of Mylanta-II liquid is 5 ml, while that of Maalox is 10 ml, the sodium content of the MRD of Mylanta-II liquid is lower than that of the MRD of any of the other Belgian liquid antacids tested.

Aluminum Hydroxide↗

Effects of three antacids on the bioavailability of valproic acid.

The effects of three antacid products on the bioavailability of valproic acid were evaluated. Each of seven normal, healthy volunteers received a 500-mg dose of valproic acid alone on one occasion and then with each of three commonly used antacids. Specifically, equal neutralizing capacity doses of 160 meq of Maalox (62 ml), Trisogel (97 ml), or Titralac (42 ml) were administered one and three hours after meals and at bedtime on the same day. Blood samples were obtained at 0, 1, 2, 4, 6, 8, 10, 24, and 32 hours and analyzed for valproic acid by gas liquid chromatography. There was a significant increase in total area under the curve (AUC) (range 3% to 28%, mean 12%) when valproic acid was administered with Maalox (p = 0.026 for total AUC and p = 0.009 for AUC to 32 hours). There was an insignificant trend toward an increase in AUC when valproic acid was administered with the other two antacids. No differences were observed in time to peak serum concentration, height of peak serum concentration, volume of distribution, half-life, or first order elimination rate constant. Caution should be exercised if valproic acid and antacids are administered concomitantly.

Adult↗

[Effect of antacids on intestinal motility].

Disturbances of gut motility occur frequently under a highdose antacid regimen. Typical symptoms are diarrhea and constipation. They are due to the cations of the antacids. Aluminum causes constipation, magnesium induces diarrhea, and calcium has no definite motor effect. The following mechanisms of action have to be taken into consideration: effects of the cations on the smooth muscle of the gut, on the enteric nervous system and on the release of gastrointestinal hormones as well as alterations of the physiochemical properties of the intraluminal contents. Aluminum inhibits the motor activity of the stomach and intestine, magnesium stimulates muscle contractions; however, the simultaneous activation of the intrinsic nerves, which are predominantly inhibitory, by magnesium may conceal the muscular effects of this cation. The diarrhea under a highdose regimen of antacid combinations appears to be due predominantly to the osmotic-secretory effects of the antacids.

Animals↗

[Effect of antacids on mineral metabolism].

Side effects of antacid therapy are dose dependant and compound related. High dose antacid intake may lead to fluid retention in the body depending on the sodium content of the different antacid preparations. Sodium bicarbonate ingestion provokes metabolic alkalosis and alkaliuria, the "nonsystemic calcium and magnesium containing antacids" cause these changes too, but to a lower degree. Urinary pH elevation favours the precipitation of calcium and magnesium salts, predisposing to renal stone formation. In patients with renal insufficiency the calcium and magnesium absorption may lead rapidly to toxic serum concentrations. Calcium and magnesium containing acids may provoke an acid rebound, which is clinically not relevant following magnesium-hydroxide-ingestion. Phosphorus depletion is an important side effect of aluminum hydroxide intake. The phosphorus depletion syndrome combined with skeletal demineralisation and osteomalacia may occur. As well as calcium and magnesium cations the tribasic aluminum will be absorbed from the gut in small amounts. In patients with renal insufficiency aluminum deposition in the brain grey matter following Al(OH)3 ingestion will occur and seems to be a co-factor for the development of a dialysis encephalopathy syndrome. The clinical relevance of aluminum absorption from gut in patients with normal renal function is unknown until now.

Alkalosis↗

The effect of antacid on gastric and duodenal bulb acidity.

A small glass pH electrode was positioned in the duodenal bulb and connected to a digital pH meter. The pH registered every half second was stored on a minidiskette with a capacity of 32.400 pH data on a single mini-disc. A microcomputer controlled electrode calibration, data collection, formating and storage. Four patients with duodenal ulcer were given a liquid test meal, and one hour later when gastric and duodenal acidity had reached high levels they were given 10 ml of antacid. From the stored pH data the mean pH and the mean hydrogen ion concentration was calculated. During the 10 min. period before antacid was given gastric pH was on average 1.5 and the duodenal pH on average 4 with a CH+ of 2.500 mumol/. Ingestion of antacid reduced gastric acidity to around pH 3, and the duodenal pH to 6 with a CH+ of 250 mumol/l. This effect of antacid was observed in all subjects, but the degree and the duration of the effect varied very much between the individuals.

Antacids↗