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PubMed1977

Circadian rhythm of urinary pH in man with and without chronic antacid administration.

In normal human volunteers, when urinary pH was plotted versus time, the circadian sine-wave type curve was not altered by chronic administration of a commercially available suspension containing a mixture of magnesium and aluminum hydroxides, although the antacid perturbed the entire curve in a more alkaline direction. A single dose of the antacid had little effect on urinary pH. There was a highly significant linear relationship between the change in hydrogen ion concentration during chronic antacid treatment and the initial control urinary hydrogen ion concentration, but there was no significant correlation between change in urinary pH and initial control urinary pH as has been previously reported. The above results were based on the evaluation of the hydrogen ion concentrations of 1562 separate urine samples collected from 24 normal subjects in a three treatment crossover study. It is recommended that: (1) research studies involving drug-drug interactions with antacids be designed to consider the effect of the antacid on the circadian rhythm of urinary pH, and (2) pH values not be averaged as commonly reported in the literature, but rather the pH values be converted to hydrogen ion concentrations before statistical analysis.

Adult↗
PubMed1982

Effects of antacids, cimetidine, and 16,16-dimethyl prostaglandin E2 on acute gastric erosions in a spinal rat.

Acute erosions of the stomach may occur in association with human spinal cord injuries. Erosion of the glandular portion of the stomach also occurs after cervical cord transection in the rat. Reports on the effects of antacids and cimetidine in the prevention of acute "stress" erosions in animals and humans have shown conflicting results. A prostaglandin analog, 16,16-dimethyl prostaglandin E2 (16,16-dmPGE2) has been shown to prevent gastric erosions in rats produced by nonsteroid antiinflammatory compounds. Cimetidine 50 mg/kg (intraperitoneal), 16,16-dmPGE2 10 micrograms/kg (intraperitoneal), and antacid 2 ml (intragastric) were individually given to groups of spinal rats at 0 and 4 hr. 16,16-dmPGE2 and antacid both resulted in significant reduction in mean ulcer length compared to controls after 8 hr (P less than 0.05) whereas cimetidine showed no significant effect, even though cimetidine caused a significant decrease in gastric acid output compared to both 16,16-dmPGE2 and controls (P less than 0.01). It is concluded that cimetidine on this dosage schedule is not effective in the prevention of gastric erosions in a cervical cord section rat model, whereas the ulceroprotective effects of 16,16-dmPGE2 and antacids are significant. It is suggested that the gastric mucosal cells remain vulnerable to injury in the cimetidine-treated spinal rat due to secretory inhibition, but are protected by buffering action of antacids or by "cytoprotective" effects of prostaglandin.

Acute Disease↗
PubMed1992

Comparison of low-dose antacids, cimetidine, and placebo on 24-hour intragastric acidity in healthy volunteers.

Low-dose aluminium (Al) antacids are effective in promoting ulcer healing and symptomatic relief in peptic ulcer patients, although the effect on intragastric acidity is very weak. In this randomized, double-blind study, 24-hr intragastric acidity was compared in 11 healthy volunteers, treated with a low-dose Al antacid regimen (1 tablet four times a day), cimetidine (800 mg at bedtime) and placebo, using the double-dummy technique. Standardized meals were given at 8 AM, noon, and 5 PM. Medication was given 1 hr after meals and at bedtime. Intragastric acidity was recorded with a nasogastric monocrystant antimony pH catheter, connected to an ambulatory digital data recorder. No significant difference in intragastric acidity was observed between antacid and placebo treatment. Treatment with cimetidine reduced circadian and nocturnal (but not diurnal) intragastric acidity significantly, as compared to both placebo and antacid treatment. The results support the hypothesis that Al antacids promote peptic ulcer healing by other mechanisms than acid neutralization.

Adult↗
PubMed1983

Cimetidine - antacid combination as premedication for elective Caesarean section.

The effect of premedication with an oral antacid (magnesium trisilicate), oral cimetidine or a combination of both was studied in 80 patients undergoing elective Caesarean section. Twenty patients served as untreated controls. Seventy per cent of the patients were in the high risk range for acid aspiration pneumonitis (pH less than 2.5 plus gastric content volume greater than 25 ml). Antacid therapy was effective in raising pH but the gastric volume remained high in 50 per cent of the patients. Cimetidine was effective in decreasing gastric volume and raising pH but the pH was still less than 2.5 in two patients. None of the patients given the cimetidine-antacid combination were in the high risk range for acid aspiration pneumonitis. The combination of an oral dose of cimetidine 400 mg, three to four hours before the operation followed by 20 ml of magnesium trisilicate one hour preoperatively proved to be the most efficacious regimen for prophylaxsis against Mendelson's syndrome in elective Caesarean section. Recent reports have suggested that non-particulate antacids (e.g., sodium citrate) may be preferable to particulate antacids such as magnesium trisilicate.

Adult↗
PubMedDate not supplied

The effects of food and of antacid on the single oral dose pharmacokinetics of tenoxicam.

A single oral dose (40 mg) of tenoxicam (Ro12-0068) was administered to six normal male volunteers pre- and post-prandially and to a further six volunteers with and without antacid to determine the effect of food and and of antacid on absorption. The rate of absorption was slower with post-prandial than with pre-prandial administration, resulting in a significantly later time for peak plasma drug levels (4.1 h compared to 1.3 h). No effect was evident on the extent of absorption or other pharmacokinetic parameters. Similarly, the rate of absorption was significantly slower after concurrent antacid than without antacid (t1/2 0.47 h compared to 0.18 h) resulting in a later peak time (4.7 h compared to 2.3 h) and significantly lower peak level (4.2 micrograms X ml-1 compared to 5.1 micrograms X ml-1) of parent drug in plasma. Again, no effect was evident on the extent of absorption or other pharmacokinetic parameters. It is concluded that food and antacids both tend to reduce the rate of absorption of tenoxicam, but that the extent of absorption is essentially unchanged. The influence on the overall kinetic profile is relatively minor, and thus unlikely to affect the therapeutic response.

Antacids↗
PubMed2003

Antacid medication inhibits digestion of dietary proteins and causes food allergy: a fish allergy model in BALB/c mice.

BACKGROUND: Digestible proteins were supposed to be irrelevant for oral sensitization and induction of food allergy. Approximately 10% of the adult population uses antacids for the treatment of dyspeptic disorders, drugs that hinder peptic digestion. In these patients, proteins that are normally degradable might act as food allergens. OBJECTIVE: We aimed to study the influence of antacid intake on the allergenicity of dietary proteins, taking sturgeon caviar and parvalbumin, the major fish allergen, as examples. METHODS: Caviar proteins and recombinant parvalbumin from carp, rCyp c 1, were applied for intragastric feedings with or without the antacids sucralfate, ranitidine or omeprazole, using a Balb/c mouse model. RESULTS: Both caviar proteins and parvalbumin were rapidly degraded in an in vitro digestion assay at pH 2.0, but not at pH 5.0, imitating the effect of antacids. The groups fed with caviar in combination with ranitidine hydrochloride intramuscularly or sucralfate orally had significant levels of caviar-specific IgE antibodies (P <.01), T-cell reactivity, and elevated counts of gastrointestinal eosinophils and mast cells. Food allergy in these groups was further evidenced by oral provocation tests and positive immediate-type skin reactivity. In contrast, feedings with caviar alone led to antigen-specific T-cell tolerance. None of the groups showed immune reactivity against the daily mouse diet. As a proof of the principle, feeding mice with parvalbumin in combination with ranitidine or omeprazole intramuscularly induced allergen-specific IgE antibodies (P <.05). CONCLUSIONS: When antacid medication impairs the gastric digestion, IgE synthesis toward novel dietary proteins is promoted, leading to food allergy.

Administration, Oral↗
PubMed1988

Persistent gastric-protective effect of antacid evaluated by measurement of transmucosal gastric potential difference.

The aim of this study was to determine the effect of 1 week of antacid dosing on the aspirin-induced potential differences (PDs) across the gastric mucosa. The study design was double blind and randomized with crossover. Ten healthy subjects received aluminum hydroxide gel, 8 gm t.i.d., or placebo for 1 week. They then received 1 gm aspirin after an overnight fast and the PD across the mucosa was measured. Baseline potentials were the same before both treatment periods. Antacids reduced the aspirin-induced PDs. The mean (+/- SD) maximal PD was 27.4 +/- 1.7 mV with placebo vs. 10.7 +/- 2.2 mV with antacids (p less than 0.001). Recovery time was 65.5 +/- 5.2 minutes with placebo vs. 29.0 +/- 6.7 minutes with antacids (p less than 0.001). These results suggest the effect is due to a longer-term cytoprotective property of antacids rather than to acid-neutralizing activity.

Adult↗
PubMed2002

The effects of cimetidine and antacid on the pharmacokinetic profile of sildenafil citrate in healthy male volunteers.

AIMS: To examine the effect of concomitant cimetidine or antacid administration on the pharmacokinetic profile of sildenafil citrate in healthy male volunteers in two open-label, randomized studies. METHODS: The first study was a parallel-group design in which 22 healthy male volunteers received sildenafil (50 mg) on days 1 and 5 and cimetidine (800 mg) or placebo on days 3, 4, 5, and 6. Blood samples were collected predose and at specified times up to 48 h postdose on days 1 and 5 to determine plasma levels of sildenafil and its metabolite, UK-103,320. The second study was a two-way crossover design in which 12 volunteers received sildenafil with or without a 30-ml dose of a magnesium hydroxide/aluminium hydroxide antacid. Blood samples were collected and analysed as in the first study. The two study periods were separated by at least 14 days. RESULTS: Coadministration of cimetidine had no statistically significant effect on the tmax or kel of sildenafil but caused a statistically significant increase in sildenafil AUCt and Cmax of 56% and 54%, respectively (P<0.01). Differences between the two treatment groups were smaller for the metabolite than for sildenafil, although cimetidine treatment did significantly (P<0.05) increase the AUCt for UK-103,320 by 30%. Antacid coadministration had no statistically significant effect on any pharmacokinetic parameter of sildenafil or UK-103,320. Whether taken alone, with cimetidine, or with an antacid, sildenafil was well tolerated. Most adverse events were mild in nature, and no subject withdrew from either study for any reason related to the drug. CONCLUSIONS: Cimetidine co-administration produced an increase in sildenafil plasma levels; however, this increase is not sufficient to warrant dosage adjustment of either drug. Antacid coadministration had no effect on the pharmacokinetic profile of sildenafil.

Adult↗
PubMed1998

Comparison of the effect of the antacid Rennie versus low-dose H2-receptor antagonists (ranitidine, famotidine) on intragastric acidity.

BACKGROUND: Symptoms of functional dyspepsia are common and patients often self-medicate with antacids, or with low-dose H2-antagonists which are available as over-the-counter medications. To date, there has been limited information available comparing the effects on intragastric acidity of these two types of over-the-counter medication. Therefore we studied the effect of the antacid Rennie and two H2-antagonists on the intragastric pH of fasting volunteers. METHODS: Sixteen healthy, fasting volunteers were randomized into a double-blind, placebo-controlled, four-way crossover study comparing Rennie (calcium-magnesium carbonate) 1360 mg, ranitidine 75 mg, famotidine 10 mg and placebo. Their effect on gastric pH was monitored by a 4-h gastric pH-metry. The primary efficacy parameter was the time lag before an intragastric pH > 3.0 was reached after drug administration. RESULTS: The median time lag before pH > 3.0 was reached after drug administration was 5.8 min for Rennie, 64.9 min for ranitidine, 70.1 min for famotidine and 240.0 min for placebo. The percentage of time with values of pH > 3.0 was 10.4% for Rennie, 61.4% for ranitidine, 56.6% for famotidine and 1.4% for placebo. CONCLUSION: The onset of action in fasting volunteers was significantly faster with the antacid than with the two H2-antagonists. The duration of action was significantly longer with an H2-antagonist than with the antacid. This suggests that the two products should be used for different indications: antacids are superior for rapid pain relief, whereas H2-antagonists might be better for symptom prophylaxis--for example for nocturnal dyspepsia.

Administration, Oral↗
PubMed2002

Lack of pharmacokinetic interaction between the oral anti-influenza neuraminidase inhibitor prodrug oseltamivir and antacids.

AIMS: Oseltamivir is an oral ester prodrug of its active metabolite Ro 64-0802, a potent and selective neuraminidase inhibitor of the influenza virus. The object of this study was to evaluate whether the oral absorption of oseltamivir was reduced in the presence of two main classes of antacid, Maalox(R) suspension (containing magnesium hydroxide and aluminium hydroxide) and Titralac(R) tablets (containing calcium carbonate). METHODS: Twelve healthy volunteers completed a randomized, single dose, three-period crossover study. Each volunteer received in a fasted state, 150 mg oseltamivir alone (Treatment A), 150 mg oseltamivir with a 20 ml Maalox suspension (Treatment B), and 150 mg oseltamivir with four Titralac tablets (Treatment C), with 7-10 days washout in between treatments. Plasma and urine concentrations of oseltamivir and Ro 64-0802 were measured using a validated h.p.l.c./MS/MS assay. Pharmacokinetic parameters were calculated for oseltamivir and Ro 64-0802. Since antacids are locally acting drugs and generally not expected to be absorbed substantially into the systemic system, no plasma or urine concentrations of antacids were measured. RESULTS: Bioequivalence was achieved for the primary pharmacokinetic parameters Cmax and AUC(0, infinity ) of Ro 64-0802 following administration of oseltamivir with either Maalox suspension or Titralac(R) tablets vs administration of oseltamivir alone. The bioavailability (90% confidence intervals) of Ro 64-0802 following administration of oseltamivir together with Maalox suspension vs administration of oseltamivir alone, was 90% (83.6, 96.9%) for C(max) and 94.1% (91.4, 96.9%) for AUC(0, infinity); similarly, for Titralac tablets, the equivalent values were 95.1% (88.3, 102%) for C(max) and 94.7% (91.9, 97.5%) for AUC(0, infinity). CONCLUSIONS: The coadministration of either Maalox suspension or Titralac tablets with oseltamivir has no effect on the pharmacokinetics of either oseltamivir or Ro 64-0802, and conversely, there is no evidence that coadministration with oseltamivir has an effect on the safety and tolerability of either Maalox suspension or Titralac tablets. There was no pharmacokinetic interaction between oseltamivir with either antacid, demonstrating that the oral absorption of oseltamivir was not impaired in the presence of antacids containing magnesium, aluminium or calcium.

Acetamides↗
PubMed1977

Healing of duodenal ulcer with an antacid regimen.

To determine whether a large-dose antacid regimen is effective in promoting healing of duodenal ulcer, 74 patients with endoscopically proved duodenal ulcer completed a 28-day double-blind clinical trial comparing such a regimen with an inert placebo. The ulcer healed completely in 28 of the 36 antacid-treated as compared to 17 of the 38 placebo-treated patients (P less than 0.005). The antacid regimen was not more effective than placebo in relieving ulcer symptoms. Presence or absence of symptoms during the fourth treatment week was a poor predictor of presence or absence of an ulcer crater. Ulcers of placebo-treated patients who smoked cigarettes were less likely to heal than those of nonsmokers (P = 0.03). Except for mild diarrhea, no side effects of the antacid regimen were observed. We conclude that a large-dose antacid regimen hastens the healing of duodenal ulcer.

Administration, Oral↗
PubMed1978

Antacid titration in the prevention of acute gastrointestinal bleeding: a controlled, randomized trial in 100 critically ill patients.

We randomized 100 critically ill patients at risk of developing acute gastrointestinal ulceration and bleeding into two groups. One (51 patients) received antacid prophylaxis, and the other (49 patients) received no specific form of prophylaxis. Hourly antacid titration kept the pH of the gastric contents above 3.5. Two of the 51 patients who received antacid prophylaxis and gastrointestinal bleeding. Twelve of the 49 control patients bled (P less than 0.005). Of the 12 patients in the control group who bled, seven were placed on antacid medication, and all seven apparently stopped bleeding. Analysis of all the patients showed that an increasing prevalence of respiratory, failure, sepsis, peritonitis, jaundice, renal failure and hypotension was correlated with a greater frequency of bleeding. No patients required operative treatment to control bleeding. These data indicate that the occurrence of acute gastrointestinal bleeding in critically ill patients can be reduced by antacid titration.

Acute Disease↗
PubMed1982

Effect of small doses of aluminum-containing antacids on calcium and phosphorus metabolism.

The effect of small doses of four commercially available aluminum-containing antacids on calcium and phosphorus metabolism was investigated in adult males in 20 studies. During the use of these doses of antacids, urinary and fecal calcium increased significantly during a low calcium intake averaging 252 mg/day, and the calcium balances became distinctly more negative. There was a reversal of the normal pattern of phosphorus excretions, namely, the fecal phosphorus was high and the urinary phosphorus was low. During a normal calcium intake of 800 mg/day, these doses of antacids did not result in significant changes of the calcium excretions or balance. Despite the decrease in net intestinal absorption of calcium, the average 47Ca absorption remained unchanged, irrespective of the type and dose of antacid used. In three patients who received large therapeutic doses of antacids, 240 to 450 ml/day, the changes of calcium and phosphorus metabolism were intensified.

Adult↗
PubMed1991

Sucralfate versus antacids or H2-antagonists for stress ulcer prophylaxis: a meta-analysis on efficacy and pneumonia rate.

OBJECTIVES AND METHODS: Histamine2 (H2)-receptor antagonists and antacids have been the basic drugs for the prevention of stress bleeding in ICU patients during the past decade. Recently, drugs without major influence on gastric pH have been investigated in stress bleeding prophylaxis. Therefore, a meta-analysis (Mantel-Haenszel test) was undertaken to determine the efficacy of sucralfate in the prevention of macroscopically visible stress bleeding, as well as the influence of sucralfate on the frequency of pulmonary infections. RESULTS: The efficacy of sucralfate was compared with H2-antagonists in nine studies and with antacids in eight studies. Sucralfate was significantly more effective than H2-antagonists (typical odds ratio 0.532, 95% confidence interval 0.303 to 0.933) and equally as effective as antacids (typical odds ratio 0.868, 95% confidence interval 0.452 to 1.667). The pneumonia rates of those patients who were administered sucralfate were compared with the rates of those patients who were given H2-antagonists in five studies and with those patients who were given antacids in four studies. Pneumonia was a significantly more frequent occurrence under prophylaxis with H2-antagonists (typical odds ratio 0.498, 95% confidence interval 0.316 to 0.783) as well as with antacids (typical odds ratio 0.402, 95% confidence interval 0.235 to 0.687). CONCLUSION: Sucralfate is an effective drug for the prevention of stress bleeding that minimizes the risk of nosocomial pneumonia in long-term ventilated ICU patients.

Antacids↗
PubMed1996

Nosocomial pneumonia in ventilated trauma patients during stress ulcer prophylaxis with sucralfate, antacid, and ranitidine.

OBJECTIVE: To compare the incidence of nosocomial pneumonia in critically injured patients randomized to one of three stress ulcer prophylaxis regimens. DESIGN: Prospective, randomized clinical trial. METHODS: Mechanically ventilated patients admitted to the trauma intensive care unit of a Level I trauma center received sucralfate, antacid, or ranitidine. MEASUREMENTS AND MAIN RESULTS: Two hundred forty-two patients were randomized: sucralfate, n = 80; antacid, n = 82; and ranitidine, n = 80. There was no statistically significant difference in pneumonia rates among the treatment groups (p = 0.875). Pneumonia occurred more frequently in patients with gram-negative retrograde colonization from stomach to trachea (p = 0.02), but this accounted for only 13% of all pneumonias in the study population. The death rate in patients with pneumonia was not statistically different among the three groups. Although 20% developed overt gastrointestinal bleeding, no episode was clinically significant. Mean gastric pH was > 4 in 95% of the study population, including 88% of patients receiving sucralfate. The death rate in the antacid group was significantly higher (p = 0.046) but not because of increased gastrointestinal bleeding or pneumonia. CONCLUSIONS: Our results show no difference in the incidence of nosocomial pneumonia in mechanically ventilated trauma patients during the first 4 days of stress ulcer prophylaxis with sucralfate, antacid, or ranitidine. There is a trend toward decreased pneumonia in the sucralfate group after study day 4. Even after controlling for injury severity, the mortality rate in the antacid group was significantly higher; the reasons for this are unknown.

Adult↗
PubMed1985

Antacids in the treatment of duodenal ulcer.

Fifty patients with endoscopically proven pyloric-prepyloric ulcers (PU/PPU) and 50 with duodenal ulcers (DU) completed a six-week double-blind clinical trial initially comprising 124 patients. The antacid-treated patients received 10 ml of an antacid suspension seven times a day (buffering 367.5 mmol acid). Healing rate after three weeks of treatment was 74% in the antacid and 42% in the placebo group (p less than 0.01). After six weeks the corresponding figures were 96 and 68% (p less than 0.001). Regarding the PU/PPU and DU subgroups we found significant differences compared to placebo in the PU/PPU group only. Antacids caused a significantly faster and more perceptible pain relief than placebo. We found no significant correlation between ulcer healing and smoking habits. Regression analyses showed that, besides antacids, ulcer size and peak acid output influenced the healing rate significantly.

Adult↗
PubMed1987

Antacid treatment of duodenal ulcer.

Sixty-seven consecutive outpatients with endoscopically verified duodenal ulcer were randomised to a double-blind treatment with either 10 ml of an antacid suspension (buffering capacity 85 mmol/10 ml, packed in single dosage pads) 1 and 3 h after each meal and at bedtime or cimetidine 400 mg b.i.d. The double-dummy technique was employed. Endoscopy was performed after 4 weeks treatment and, if the ulcer had not healed, after 8 weeks treatment. When ulcer healing had occurred, the patient entered a 1 year follow-up study. The cumulative healing rates after 4 and 8 weeks treatment were 83 and 97% vs. 69 and 94% in the antacid and cimetidine groups respectively. No significant differences were observed between the treatment groups regarding ulcer healing, symptom relief or compliance. Adverse reactions were few and only 3 (9%) patients in the antacid group had to discontinue the treatment due to diarrhoea. Of the cimetidine treated patients, 61% had symptomatic relapse during the 1 year follow-up compared to 71% of the antacid treated patients. There were no significant differences in recurrence rate or time to relapse. The moderate dose antacid treatment used here is efficient, well tolerated, safe, convenient and is a good alternative treatment of the duodenal ulcer patient.

Adult↗
PubMed1988

A model of an 'artificial stomach' for assessing the characteristics of an antacid.

A model of an 'artificial stomach' has been constructed in order to take into account some of the parameters lacking in conventional in vitro antacid evaluation, namely the interaction between secretory flux and variation in emptying fluxes, the presence of proteins, and the use of human gastric juice instead of an aqueous solution of hydrochloric acid. The 'artificial stomach' has two elements, the 'stomach' and the pH recording system. The 'stomach' includes a 'gastric' reservoir receiving secretory flux and is emptied by variable fluxes. Aluminium phosphate gel has been studied in 100 ml of 0.1 N HCl, without and with 1 or 5% meat extracts and also in 100 ml of human gastric juice. The antacid effect of 1 or 5% meat extracts has also been assessed. The antacid effect of aluminium phosphate was characterized by the pH rise of the 'gastric' contents, the buffering capacity, and the dilution of gastric contents. These factors were modulated by emptying fluxes. The same characteristics were found when antacid was studied in gastric juice. Proteins exerted a neutralizing effect and modified aluminium phosphate's antacid capacity. A mechanism for buffering capacity by cation aluminium is suggested.

Antacids↗