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UNLABELLED: Accurate measurement of intragastric acidity has both clinical and investigational importance in studying gastric pathophysiology. OBJECTIVES: The aims of this study were fourfold: (1) to investigate whether regional differences in intragastric acidity exist; (2) to determine intragastric acidity after a standard antacid was administered in both the fasting and fed states; (3) to monitor gastric emptying of and anatomic distribution of radiolabeled antacid during fasting and postprandial periods; and (4) to determine whether the regional effects of ingested antacid correlated with the anatomic distribution of the antacid. METHODS: Eight normal male volunteers were studied after fluoroscopically guided nasogastric placement of a tube assembly containing four pH electrodes, with one electrode in each quartile of the stomach. Simultaneous pH readings were made from the four electrodes while fasting, after administration of fasting antacid (30 ml, 79 mEq buffering capacity), postprandially, and after postprandial antacid ingestion. All subjects repeated the protocol on a separate day, five of them using radiolabeled antacid. Gastric emptying and gastric distribution over time of radiolabeled antacid were determined for comparison to regional intragastric acidity. RESULTS: Intragastric acidity varied regionally over time in response to meals and to fasting and postprandial antacid. In the fasting state, intragastric acidity returned to baseline after antacid ingestion in a proximal to distal (cardia to antrum) sequence, while postprandial antacid resulted in a return to baseline acidity in a distal to proximal (antrum to cardia) sequence. Radiolabeled antacid distribution paralleled intragastric pH and hydrogen ion concentration in the fasting state, with 82% of the antacid localizing in the distal half of the stomach within the first minute after antacid ingestion. Postprandially, the greatest initial and most prolonged antacid buffering effect occurred proximally, correlating with the presence of radiolabeled antacid. Postprandial antacid remained in the stomach for a longer time (T1/2 = 93.1 +/- 23.4 min) compared with fasting antacid (T1/2 = 23.6 +/- 11.1 min). CONCLUSIONS: Measurement of acidity in the four quartiles of the stomach demonstrated regional variation in response to both food and a standard antacid. A single pH electrode does not detect regional intragastric pH differences.
A valid in vitro evaluation of antacid capacity should consider: 1) the intragastric pH-range; 2) the antacid mechanism; 3) the dependence of antacid activity from intraluminal flux variations; 4) the interaction between proteins and antacids. Pharmacologically, a static method allows 1) to quantify H+ binding sites at different pH-end points of the titration: pH 3.0, 2.0 and 1.0 and 2) to characterize the antacid mechanism, neutralizing activity and/or buffering capacity. In dynamic conditions, using the "artificial stomach-duodenum" model the antacid-induced resistance to acidification was measured, the antacid mechanisms were characterized in regard to intraluminal gastroduodenal flux variations and the incidence of antacid activity on duodenal pH was evaluated. These procedures were applied to antacid evaluation of proteins, as natural antacids, and of drugs containing aluminium salts alone or combined with magnesium salts. Pharmacologically, antacid drugs exhibited a greater amount of H+ binding sites when titration end-point was pH 1.0 than pH 3.0 corresponding to the development of neutralizing activity and/or buffering capacity. In dynamic conditions, the drugs, like proteins, induced a potent resistance to acidification related to gastric emptying fluxes. Antacid effect was supported by neutralizing activity and/or by buffering capacity. It was prolonged by removal of H+ ions since lagtimes for recovering initial pH were longer than antacid total emptying, the dilution of intragastric content by H+ impoverished secretory flux contributing thus to prevent gastric acidification. At duodenal site, proteins and aluminium-containing antacids induced the same duodenal pH as controls, without antacids, while magnesium-containing antacids increased it.
BACKGROUND: Although antacids are popular drugs with a long history of use, their true utilization patterns-including over-the-counter use-have rarely been documented. Because all antacids are reimbursed under the National Health Insurance program in Taiwan, it is possible to access and analyze nationwide data for these drugs. OBJECTIVES: The purposes of this study were to estimate the scale of antacid prescribing in Taiwan using the national insurance claims for outpatient services and to analyze coprescribing patterns of antacids using modern data-mining techniques. METHODS: The National Health Insurance Research Database in Taiwan supplied the visit-based sampling data sets, which had a sampling ratio of 0.2% for all claims for outpatient medical services in the year 2000. In addition to the plain statistics (ie, data from simple calculations) for antacid prescriptions, we also analyzed relationships between prescriptions for antacids and nonantacid drugs. A data-mining technique-association rule mining-was applied to identify the drugs prescribed in combination with antacids. RESULTS: Among a total of 409,049 eligible prescriptions for 1,704,595 drug items to be administered orally, antacids were present in 213,494 prescriptions (52.2%). Antacid users were generally older than nonusers (mean [SD] age, 39.9 [23.4] years vs 32.4 [25.7] years). In all, 88.8% of antacid items (189,531/213,494) were prescribed without claims diagnoses of gastrointestinal disorders. Using association rule mining with a 1.0% minimum support factor, there were 36 strong association rules between prescriptions for antacids and other drug subgroups at the third level of Anatomical Therapeutic Chemical classification. Nonsteroidal anti-inflammatory drugs and drugs for treating upper respiratory infections played dominant roles in the associations with antacid prescriptions; vitamin B complex and antivertigo preparations were also strongly associated with antacids. CONCLUSIONS: Antacid coprescriptions were common in Taiwan in the year 2000. Further study should investigate whether antacid prescribing patterns are influenced by Taiwanese perceptions that Western drugs injure the stomach.
Self-medication with antacids is very common in patients with less severe forms of dyspepsia, but we know very little about the users of antacids and their incentive to take them. The aim of this study was to analyze the relationship between self-reported use of antacids and health-related variables, lifestyle, and sociodemographic characteristics in order to characterize the use of antacids in a general population. The use of antacids was assessed by a questionnaire answered by men and women aged 20-62 years (n = 15,986; response rate 75.9%). Logistic regression analysis was used to quantify the relationships between the use of antacids and health-related variables, lifestyle, and sociodemographic characteristics. Approximately 10% of the population had used antacids during the preceding 14 days. There was no overall gender difference. Among those who had no dyspeptic symptoms, 1.5% reported use of antacids, whereas among those who had all three dyspeptic symptoms (heartburn, epigastric pain, peptic ulcer), 46.5% had used antacids. Heartburn was the most important predictor for antacid use in both men (odds ratio [OR] = 8.57 [6.65-11.04]) and women (OR = 9.35 [7.16-12.221) followed by self-reported epigastric pain and peptic ulcer (both: OR = approximately 2). The importance of these self-reported health conditions remained unchanged after adjusting for lifestyle and sociodemographic variables. There were fewer antacid users among unmarried women than married women, and coffee-drinking was inversely associated with antacid use. These findings were consistent in both bivariate and multivariate analysis. The present study provides population-based information showing that self-medication with antacids in Norway appeared to be appropriate. Because dyspeptic symptoms play a major role in the consumption of antacids, this study shows the importance of including information about specific clinical variables in the analysis and interpretation of patterns of drug use.
Antacids have served us well for over a century. In terms of peptic ulcer disease, the attitude in the late 1950s to 1970s that antacids should be taken only on demand was unjustified and erroneous. 13 recent endoscopic controlled studies have confirmed the efficacy of antacids in the healing of duodenal ulcer, achieving about 75% healing in 4 weeks. The efficacy of antacids in promoting gastric ulcer healing has been less well studied and the results are controversial. The most appropriate and economical antacid regimens for the treatment of duodenal ulcer disease should include tablets or liquid that have acid neutralising capacity of 400 mmol/day given at least an hour after meals. As a long term therapy, antacids appear to work, but need be taken in multiple daily doses, a regimen which is unlikely to meet with long term patient compliance. Patients with gastro-oesophageal reflux disorders or pregnancy-related reflux have also benefited from the usage of antacids ad libitum. Early previous studies have clearly demonstrated the efficacy of antacids in reducing gastro-oesophageal reflux and healing of reflux oesophagitis. The acidity of the gastric contents is the major determining factor in the outcome of the aspiration pneumonitis occurring during delivery. The prophylactic use of antacids during delivery has helped to reduce the severity of this complication. Similarly, the prophylactic administration of antacid aiming to maintain gastric pH between 3.5 to 7.0 has resulted in significant reduction of bleeding due to stress associated ulcers and/or erosive haemorrhagic gastritis in critically ill patients. Antacid therapy, however, is controversial in the management of nonulcer dyspepsia or nonsteroidal anti-inflammatory drug related upper gastrointestinal mucosal damage. Undoubtedly, antacids have major roles to play in the treatment of gastric acid related disorders. They have clear advantages and disadvantages when compared with the antisecretory agents. New proton pump inhibitors in particular have certainly superseded antacids and even the H2-receptor antagonists in many respects. However, the long term safety record of antacids remains unsurpassed by any of the new antisecretory agents.
Since a previous review by Hurwitz was published in 1977 a large number of reports on drug interactions with antacids have appeared, few of which are of clinical relevance. Tetracyclines form insoluble complex molecules by metal ion chelation with various antacids; tetracycline absorption may be decreased by more than 90% by this interaction. Of the new class of quinolone antibiotics, the absorption of ciprofloxacin and ofloxacin is reduced by 50 to 90% in the presence of aluminium- and magnesium hydroxide-containing antacids. In contrast to early work showing inhibition of the absorption of beta-adrenergic blocking drugs by antacids, subsequent studies did not confirm a reduction in the bioavailability of either atenolol or propranolol during antacid treatment; indeed, they showed an increase in the plasma concentrations of metoprolol when the drug was coadministered with an antacid. The bioavailability of captopril was significantly reduced in the presence of an antacid, and lower plasma concentrations of this angiotensin-converting enzyme inhibitor were accompanied by a reduction of its effect on the systolic blood pressure of the patients. The absorption of the cardiac glycosides digoxin and digitoxin is not inhibited by antacids to a significant degree, although earlier studies had shown a positive effect when the dissolution of the glycoside preparations was relatively poor. Antacids reduce the bioavailability of the H2-receptor antagonists cimetidine and ranitidine only when high antacid doses are used and when the drugs are administered simultaneously. The bioavailability of famotidine was not significantly altered by a potent antacid preparation, although a trend towards reduced absorption was observed. Iron absorption is significantly decreased in the presence of sodium bicarbonate and calcium carbonate, but is nearly complete when coadministered with aluminium-magnesium hydroxide. Nonsteroidal anti-inflammatory drugs such as naproxen, tenoxicam, ketoprofen, ibuprofen and piroxicam are not affected in their absorption by antacid treatment. Theophylline bioavailability is unchanged when the drug is given together with antacids, although its rate of absorption may be altered, leading to a reduction or an increase in the time of the occurrence of peak plasma drug concentrations.
To improve the dynamic in-vitro evaluation of the effects of antacids, we have developed the 'artificial stomach' model by adding a 'duodenal reservoir' to receive the gastric emptying flux and simulated bicarbonate secretion, thus constituting an 'artificial stomach-duodenum' model. With this model we measured antacid-induced resistance to gastric acidification, and simultaneously evaluated the effect of antacid activity on the duodenal milieu. The model also permitted evaluation of the antacid effects of proteins (as natural antacids), and of drugs containing aluminium phosphate, alone or combined with magnesium oxide, or aluminium and magnesium hydroxides. At the gastric site, these drugs, as well as the proteins (that is, meat extract), induced a strong resistance to acidification due to the gastric emptying flux and to antacid composition. At the duodenal site, the decrease of the acid load penetrating into the duodenum varied, depending on the efficacy of gastric antacid activity. Duodenal pH was related to the equilibrium between bicarbonate secretion and the emptying of acid load. Proteins and aluminium phosphate induced the same duodenal pH as in the control tests without antacids, but magnesium-containing antacids increased it, thus decreasing bicarbonate consumption. The antacid mechanisms within the stomach, and the fate of antacids in the duodenal milieu, might explain the variation in duodenal pH in response to antacid administration.
Antacids are commonly used self-prescribed medications. They consist of calcium carbonate and magnesium and aluminum salts in various compounds or combinations. The effect of antacids on the stomach is due to partial neutralisation of gastric hydrochloric acid and inhibition of the proteolytic enzyme, pepsin. Each cation salt has its own pharmacological characteristics that are important for determination of which product can be used for certain indications. Antacids have been used for duodenal and gastric ulcers, stress gastritis, gastro-oesophageal reflux disease, pancreatic insufficiency, non-ulcer dyspepsia, bile acid mediated diarrhoea, biliary reflux, constipation, osteoporosis, urinary alkalinisation and chronic renal failure as a dietary phosphate binder. The development of histamine H2-receptor antagonists and proton pump inhibitors has significantly reduced usage for duodenal and gastric ulcers and gastro-oesophageal reflux disease. However, antacids can still be useful for stress gastritis and non-ulcer dyspepsia. The recent release of proprietary H2 antagonists has likely further reduced antacid use for non-ulcer dyspepsia. Other indications are still valid but represent minor uses. Antacid drug interactions are well noted, but can be avoided by rescheduling medication administration times. This can be inconvenient and discourage compliance with other medications. All antacids can produce drug interactions by changing gastric pH, thus altering drug dissolution of dosage forms, reduction of gastric acid hydrolysis of drugs, or alter drug elimination by changing urinary pH. Most antacids, except sodium bicarbonate, may decrease drug absorption by adsorption or chelation of other drugs. Most adverse effects from antacids are minor with periodic use of small amounts. However, when large doses are taken for long periods of time, significant adverse effects may occur especially patients with underlying diseases such as chronic renal failure. These adverse effects can be reduced by monitoring of electrolyte status and avoiding aluminum-containing antacids to bind dietary phosphate in chronic renal failure. Antacids, although effective for discussed indications of duodenal and gastric ulcer and gastro-oesophageal reflux disease, have been replaced by newer, more effective agents that are more palatable to patients. Antacids are likely to continue to be used for non-ulcer dyspepsia, minor episodes of heartburn (gastro-oesophageal reflux disease) and other clear indications. Although their wide-spread use may decline, these drugs will still be used, and clinicians should be aware of their potential drug interactions and adverse effects.
The prescribing physician is faced with a wide choice of antacid preparations. To provide a guide, we tested the commonly available antacids, both liquid and tablet, for their acid-neutralizing capacity. We calculated the cost effectiveness of antacids and tabulated the cost of 1 month of therapy. The acid-neutralizing capacity and cost effectiveness of liquid antacids are generally better than tablet antacids. The most effective liquid antacids, which are composed of either aluminum and magnesium hydroxide mixtures or calcium carbonate, vary in buffering capacity from 3 to 4.2 meq/mL of antacid and range in monthly cost of therapy from $35 to $74. In contrast, the five least effective liquid antacids vary in acid-neutralizing capacity from 0.3 to 2.3 meq/mL of antacid and in monthly cost of therapy from $78 to $498. Because the monthly cost of therapy is influenced primarily by the acid-neutralizing capacity of the antacid, a high-potency antacid should be prescribed. The taste and sodium content of the antacids should also be taken into account by the prescribing physician.
BACKGROUND: Heartburn, a common symptom, is self-treated with oral antacids. Efficacy of antacids has not been demonstrated for individual, spontaneous heartburn episodes. METHODS: We conducted a double-blind, randomized, placebo-controlled, parallel-group study of self-directed treatment for episodic heartburn comparing famotidine (FAM) 5, 10, or 20 mg and antacid (11 mEq ANC) to placebo (PBO) during a 4-week period. Twenty-nine US investigators enrolled a total of 565 outpatients, ages 18--81 years (mean 44.1 years) with heartburn but not seeking care for heartburn. Treatment of spontaneous heartburn episodes was permitted as needed, up to twice daily, with self-administered test drug. An open-label, backup antacid was provided to use if test drug did not provide adequate relief. Patients assessed heartburn relief hourly and recorded use of backup antacid. Relief was defined as complete relief of symptoms without the use of backup antacid. RESULTS: The media proportion of episodes relieved was: PBO, 41%; FAM 5 mg, 59%, 0.05 less-than-or-equal p < 0.10; FAM 10 mg, 70%, p < 0.001; FAM 20 mg, 69%, p < 0.001; antacid, 62%, p < 0.05 (p-values versus PBO). Supplemental analyses incorporating time to relief confirmed that famotidine and antacid provided more rapid and more frequent relief than placebo (odds ratio for relief relative to PBO: FAM 5 mg, 1.55, p = 0.003; FAM 10 mg, 1.94, p < 0.001; FAM 20 mg, 2.13, p < 0.001; antacid 1.57, p = 0.003). The tolerability profile was similar with famotidine, antacid, and placebo. CONCLUSIONS: The positive results with antacid demonstrated for the first time the efficacy of antacid in self-treatment of individual heartburn episodes and provided internal validation of this study paradigm. Patients in this study self-medicated effectively using low doses of famotidine on an as needed basis for spontaneous episodes of heartburn.