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Objective: The 13 C-urea breath test (UBT) is the most widely used non-invasive diagnostic test for Helicobacter pylori. Debate continues to surround the possible interference of antacid intake on its result. This study aims to confirm the non-interference of almagate in the determination of H. pylori by UBT., Patients and Methods: Observational, multicentre study in adult patients treated with almagate in whom a UBT (TAUKIT®) was indicated. When the UBT result was negative, use of almagate was stopped for 30 days and the UBT was repeated. When the result was positive, no further determinations were made. The primary endpoint was the percentage of patients who, having had a negative result in the first breath test, were positive in the second after having stopped taking almagate (UBT false negatives, possibly attributable to almagate)., Results: Of the 167 evaluable patients, 59% were female, average age was 49 and 97% had gastrointestinal symptoms. The result of the first UBT was negative in 71% of cases. Of these, in the second UBT test after stopping the almagate, the negative result was confirmed in 97.5%. Out of the total number of cases evaluated, the rate of false negatives was 1.8%., Conclusions: Taking almagate has minimal or no interference in the result of UBT for the diagnosis of H. pylori infection. It can therefore be used in the weeks prior to a UBT., (Copyright © 2021 The Authors. Publicado por Elsevier España, S.L.U. All rights reserved.)

Introduction: Increasing dialysate magnesium (D-Mg 2+ ) appears to be an intriguing strategy to obtain cardiovascular benefits in subjects with end-stage kidney disease (ESKD) on hemodialysis. To date, however, hemodialysis guidelines do not suggest to increase D-Mg 2+ routinely set at 0.50 mmol/L., Methods: A randomized 4-week crossover study aimed at investigating the consequences of increasing D-Mg 2+ from 0.50 to 0.75 mmol/L on arterial stiffness, hemodynamic profile, and endothelial function in subjects undergoing hemodialysis. The long-term effect of higher D-Mg 2+ on mineral metabolism markers was investigated in a 6-month follow-up. Data were analyzed by linear mixed models for repeated measures., Results: Data of 39 patients were analyzed. Pulse wave velocity and pulse pressure significantly decreased on the higher D-Mg 2+ compared with the standard one by - 0.91 m/s (95% confidence interval - 1.52 to - 0.29; p = 0.01) and - 9.61 mmHg (- 18.89 to - 0.33, p = 0.04), respectively. A significant reduction in systolic blood pressure of - 12.96 mmHg (- 24.71 to - 1.22, p = 0.03) was also observed. No period or carryover effects were observed. During the long-term follow-up phase the higher D-Mg 2+ significantly increased ionized and total serum Mg (respectively from 0.54 to 0.64 and from 0.84 to 1.07 mmol/L; mean percentage change from baseline to follow-up + 21% and + 27%; p ≤ 0.001), while parathormone (PTH) decreased significantly (from 36.6 to 34.4 pmol/L; % change - 11%, p = 0.03)., Conclusions: Increasing dialysate magnesium improves vascular stiffness in subjects undergoing maintenance hemodialysis. The present findings merit a larger trial to evaluate the effects of 0.75 mmol/L D-Mg 2+ on major clinical outcomes., Trial Registration: The study was retrospectively registered on the ISRCTN registry (ISRCTN 74139255) on 18 June 2020.

Objectives: Raltegravir is a human immunodeficiency virus (HIV)-1 integrase strand transfer inhibitor currently marketed at a dose of 400 mg twice daily (BID). Raltegravir for once-daily regimen (QD) at a dose of 1200 mg is under development. The effect of calcium carbonate and magnesium/aluminium hydroxide antacids on the pharmacokinetics of a 1200 mg dose of raltegravir was assessed in this study., Methods: An open-label, four-period, four-treatment, fixed-sequence study in 20 HIV-infected patients was performed. Patients needed to be on raltegravir as part of a stable treatment regimen for HIV, and upon entry into the trial received 5 days of 1200 mg raltegravir as pretreatment, before they entered the four-period study: 1200 mg of raltegravir alone (period 1), calcium carbonate antacid as TUMS ® Ultra Strength (US) 1000 and 1200 mg raltegravir given concomitantly (Period 2), magnesium/aluminium hydroxide antacid as 20 ml MAALOX ® Maximum Strength substitute MS given 12 h after administration of 1200 mg raltegravir (period 3), and calcium carbonate antacid as TUMS ® US 1000 given 12 h after administration of 1200 mg raltegravir (period 4). Patients received their dose of 1200 mg QD raltegravir during the intervals between periods to re-establish steady state. AUC 0-24 , C 24 , C max and T max were calculated from the individual plasma concentrations of 1200 mg QD raltegravir after administration alone or with a calcium carbonate antacid or with a staggered dose of a calcium carbonate antacid or magnesium/aluminium hydroxide antacid. Adverse events, in addition to laboratory safety tests (haematology, serum chemistry and urinalysis), 12-lead electrocardiograms and vital signs were assessed., Key Findings: All treatments were well tolerated in the study. Metal-cation antacids variably affected the pharmacokinetics of 1200 mg QD raltegravir. When calcium carbonate antacid was given with 1200 mg raltegravir concomitantly, the geometric mean ratio (GMR) and its associated 90% confidence interval (90% CI) for AUC 0-24 , C max and C 24 h were 0.28 (0.24, 0.32), 0.26 (0.21, 0.32) and 0.52 (0.45, 0.61), respectively. When calcium carbonate antacid and magnesium/aluminium hydroxide were given 12 h after raltegravir 1200 mg QD dosing, the GMR (90% CI) values for AUC 0-24 and C max were 0.90 (0.80, 1.03), 0.98 (0.81, 1.17), and 0.86 (0.73, 1.03), 0.86 (0.65, 1.15), respectively. However, significant reduction in the trough concentrations of raltegravir was observed: C 24 h 0.43 (0.36, 0.51) in the presence of calcium carbonate antacids and 0.42 (0.34, 0.52) in presence of magnesium/aluminium hydroxide, respectively., Conclusions: Overall, the use of metal-cation antacids with 1200 mg QD raltegravir is not recommended., (© 2016 Royal Pharmaceutical Society.)

This clinical case and the literature review show possible development of methemoglobinemia due to the use of local anesthetics, included in drugs for the gastrointestinal diseases treatment, in particular benzocaine, which is the methaemoglobin forming agent. These drugs are common and often taken by the patients themselves without any control. The aim of our paper is to draw the attention of physicians to the risk of the widely known drug administration which can be purchased without a prescription.

The aim of this work was to develop new mucoadhesive buccal patches containing an inorganic fluorinated compound, MgAl-F, intended for decay prevention. Firstly MgAl-F was synthesized and characterized, then the patches were prepared starting from a physical blend of mucoadhesive polymers (NaCMC and polycarbophil) in which MgAl-F was dispersed in different amounts in order to obtain the films. The prepared mucoadhesive patches were characterized in terms of swelling capacity, mucoadhesion force and time, surface morphology and in vitro release studies. Moreover, the organoleptic properties and acceptability have been evaluated by in vivo application. The performed studies demonstrated that the proposed formulations are practical, manageable, flexible and adaptable to the biological substrate showing, at the same time, good organoleptic properties. Moreover, the presence of the MgAl-F is able to decrease the strong adhesion of the employed polymers, reducing pain and irritations resulting in a high patient acceptability. Data obtained from release studies revealed that the application of small patch portions is enough able to release, for a prolonged time, an amount of fluoride ions able to reach the efficacious dose. These observations suggest the applicability of such formulations for buccal administration of different active ingredients., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Objective: The aim of the study was to investigate whether hydrotalcite was comparable to esomeprazole, a proton pump inhibitor, in on-demand therapy for non-erosive reflux disease (NERD)., Methods: This was a multicenter, randomized, open-label clinical trial with initial and on-demand therapy. Patients who had complete symptom relief in the initial therapy were randomized to either hydrotalcite or esomeprazole in the on-demand therapy. The percentage of patients who quit on-demand therapy in the two groups and the cost-effectiveness of the treatment were evaluated as primary end points. The rate of symptom relief and the improvement of symptom score for initial therapy and the weekly average symptom score and weekly average number of days on treatment for on-demand therapy were evaluated as secondary end points., Results: In total, 398 patients were recruited in the initial therapy group, among whom 253 were included in on-demand therapy, with 127 patients in the hydrotalcite group and the remaining 126 in the esomeprazole group. 14 (11.0%) patients in the hydrotalcite group and six (4.8%) in the esomeprazole group quit the on-demand therapy due to unsatisfactory symptom control (P = 0.065). Cost-effectiveness calculated as the ratio of the cost of hydrotalcite to that of esomeprazole (per person/day) was 35.3% in the on-demand therapy. Similar number of patients achieved symptom relief in both groups., Conclusion: Hydrotalcite is a good option of on-demand therapy for NERD patients due to its cost-effectiveness and speed of action., (© 2013 Wiley Publishing Asia Pty Ltd and Chinese Medical Association Shanghai Branch, Chinese Society of Gastroenterology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine.)

We report on a scrub typhus patient who contracted meningoencephalitis during doxycycline administration. This is the first case of scrub typhus in which doxycycline concentrations were measured in serum and cerebrospinal fluid. Clinicians should be alerted to the possibility that meningoencephalitis can occur because of inadequate maintenance of serum doxycycline level caused by antacids administered along with doxycycline., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Objective: Rosuvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor used for the treatment of dyslipidaemia, may be co-administered with antacids in clinical practice. This trial assessed the effect of simultaneous and separated administration of an antacid preparation containing aluminium hydroxide 220 mg/5 mL and magnesium hydroxide 195 mg/5 mL (co-magaldrox 195/220) on the pharmacokinetics of rosuvastatin., Research Design and Methods: A randomised, open-label, three-way crossover trial was performed. Healthy male volunteers (n = 14) received a single dose of rosuvastatin 40 mg alone, rosuvastatin 40 mg plus 20 mL antacid suspension taken simultaneously, and rosuvastatin 40 mg plus 20 mL antacid suspension taken 2 h after rosuvastatin on three separate occasions with a washout of > or = 7 days between each., Main Outcome Measures: The primary parameters were area under the rosuvastatin plasma concentration-time curve from time zero to the last quantifiable concentration (AUC(0-t)) and maximum observed rosuvastatin plasma concentration (C(max)) in the absence and presence of antacid., Results: When rosuvastatin and antacid were given simultaneously, the antacid reduced the rosuvastatin AUC(0-t) by 54% (90% confidence interval [CI] for the treatment 0.40-0.53) and C(max) by 50% (90% CI 0.41-0.60). When the antacid was given 2 h after rosuvastatin, the antacid reduced the rosuvastatin AUC(0-t) by 22% (90% CI 0.68-0.90) and the C(max) by 16% (90% CI 0.70-1.01). The effect of repeated antacid administration was not studied and it cannot be discounted that this may have resulted in a stronger interaction than that observed here., Conclusions: Simultaneous dosing with rosuvastatin and antacid resulted in a decrease in rosuvastatin systemic exposure of approximately 50%. This effect was mitigated when antacid was administered 2 h after rosuvastatin.

Background: Postoperative atrial fibrillation has been refractory to many attempted pharmacologic prevention methods and, when effective, side effects have been described. The present aim was to study the clinical compliance of a suggested prophylactic treatment, oral sotalol, and magnesium., Methods: Coronary-bypass patients without clinical contraindications to receive oral sotalol (80 mg twice daily) and magnesium supplementation were enrolled (n = 49) with an intention-to-treat strategy and being compared with a matched control group (n = 844). A protocol listed exclusion criteria of clinical compliance that was postoperatively evaluated prior to and during treatment., Results: Twenty-seven of the 49 enrolled patients (55%) were compliant to sustain the treatment according to the protocol. The remaining patients were postoperatively excluded, mainly because of hemodynamic reasons, of whom 14 were noncompliant to initiate any treatment. The AF occurrence in the compliant group was 7% versus 36% in noncompliant patients (p = 0.035), and 24% in the control group (p = 0.076). However, with an intention-to-treat policy the overall AF incidence became 18%. The subgroups of enrolled patients demonstrated skewing phenomena. The noncompliant group had higher requirement for inotropic support (p = 0.029) and longer aortic cross-clamp time (p = 0.048) compared to compliant patients. Further, the body weight of noncompliant patients was markedly lower than in the compliant counterpart (p = 0.015)., Conclusions: The tested treatment protocol showed limited compliance among routine cardiac-surgery patients, and further, introduced a biased selection of patients that skewed the results and may have partly explained the treatment effect.

Non-prescribed antacid drugs that contain magnesium and aluminum are widely used in the treatment of gastritis and peptic ulcer. One of the side effects of these antacid drugs is that they bind phosphate in the gut and result in its malabsorption. In this paper, a 42-year-old female patient who used magnesium hydroxide (Magnesie calcinee powder 100 g) to benefit from its laxative feature, and developed osteomalacia after losing 90 kg in 2 years will be presented by going through the related literature. She had widespread joint pain and could hardly walk without the help. Ca, P and vitamin D were at lower limit of normal, ALP, Mg and PTH were increased in her laboratory tests. There were stress fractures at the femur neck and at the upper part of the tibia in plane radiographies. The patient was hospitalized with the diagnosis of osteomalacia and she was treated successfully.

Sparfloxacin is a broad-spectrum oral fluoroquinolone antimicrobial agent with a long elimination half-life (t(1/2)). Concurrent treatment with antacids has demonstrated a reduction in the oral absorption of many quinolones. This study was undertaken to determine an optimal time for dosing antacids in relation to sparfloxacin administration to minimize antacid-induced reduction in sparfloxacin bioavailability. This open-label, single-dose, randomized, four-way crossover study was conducted in 20 healthy male volunteers between the ages of 18 and 38 years. Treatments consisted of single 400-mg oral doses of sparfloxacin alone and with Maalox 30 mL given 2 hours before, 2 hours after, and 4 hours after oral administration of sparfloxacin. All 20 subjects completed the study. A 400-mg single oral dose of sparfloxacin was well tolerated both given alone and with Maalox. Maalox given 4 hours after sparfloxacin administration was the only regimen that did not cause a statistically significant reduction in the rate and extent of sparfloxacin absorption. The 90% confidence intervals comparing sparfloxacin alone with the preceding regimen in terms of area under the concentration-time curve from zero to infinity (AUC(0-infinity)) and maximum plasma concentration (Cmax) were within the range 80% to 125%. Administration of Maalox 2 hours before, 2 hours after, and 4 hours after sparfloxacin caused mean decreases in AUC(0-infinity) of 23%, 17%, and 5%, respectively. Corresponding decreases in mean Cmax values were 29% with Maalox administered 2 hours before sparfloxacin and 13% with Maalox administered 2 hours after sparfloxacin. The mean Cmax value was un affected when Maalox was administered 4 hours after sparfloxacin administration. The 90% confidence intervals for these comparisons with sparfloxacin alone were outside the 80% to 125% range and did not include 100%. Time to Cmax and t(1/2) were similar for all four regimens. The elimination rate of sparfloxacin was unaffected by concomitant administration with Maalox in healthy male volunteers.

Background: Antacids, such as aluminium-magnesium hydroxide (AIMg(OH)3), or H2-receptor antagonists, such as ranitidine, are common drugs used for treating peptic ulcer disease and acid-related symptoms., Methods: In a prospective double-blind controlled study, 174 patients were randomized to a 4-week course of treatment with either AIMg(OH)3 (acid-binding capacity: 280 mval/day) or ranitidine 300 mg for active Helicobacter pylori-associated duodenal ulcers (as determined by histology and the urease test). Before and after treatment, two biopsy specimens each were obtained from the antrum and corpus, and the grade and activity of gastritis, as well as H. pylori density, were determined using a score ranging from 0 = none to 4 = severe., Results: Pre- and post-treatment histology were available for 138 patients (AIMg(OH)3: 67, ranitidine; 71). Treatment with AIMg(OH)3 significantly increased the activity of corpus gastritis (Wilcoxon signed-rank: P = 0.0014), while ranitidine treatment significantly increased both the grade and activity of corpus gastritis (P = 0.0002 and P = 0.0001 respectively). In the antrum, both regimens provoked a significant increase in the frequency of intestinal metaplasia, but this may be a consequence of sampling error., Conclusions: Ranitidine and AIMg(OH)3 have an aggravating effect on H. pylori gastritis in duodenal ulcer patients. This should be considered a side-effect of the respective drugs and is more pronounced with ranitidine.

Meloxicam is a new enol carboxamide nonsteroidal antiinflammatory drug (NSAID). Preclinical studies have indicated that it possesses a high antiinflammatory potency and a low ulcerogenic potency. This open, randomized, crossover study was conducted to examine the effects of aspirin, the antacid Maalox (Rhone-Poulenc Rorer, Cologne, Germany), and cimetidine on the pharmacokinetics and bioavailability of a single oral dose of meloxicam 30 mg in healthy male volunteers. Plasma concentrations of meloxicam were determined and subjected to noncompartmental pharmacokinetic analysis. Meloxicam was well tolerated, and concomitant treatment with cimetidine or Maalox had little or no effect on the plasma concentration-time curves, maximum plasma concentration (Cmax), or the area under the plasma concentration-time curve (AUC0-infinity) of meloxicam. Concurrent treatment with aspirin increased plasma concentrations of meloxicam, increasing Cmax by approximately 25% and AUC0-infinity by 10%. These differences were not considered to be clinically relevant, and no adjustments of meloxicam dose should be required with coadministration of aspirin, Maalox, or cimetidine.

A premature infant with severe enteroviral infection was treated with Maalox for gastric bleeding. Bezoars formed, which were shown to contain high concentrations of magnesium. An association between antacid administration and bezoar formation in neonates has been previously suggested but has not until now been clearly documented.

Two infants presented with growth failure and were found to have generalized osteomalacia (rickets) due to phosphate depletion from prolonged administration of an aluminum-containing antacid given for the symptoms of colic. One of the infants developed bilateral proptosis due to craniosynostosis related to the underlying metabolic bone disease. The chronic use of aluminum-containing antacids in infants has potential risk for the growing skeleton and is not innocuous. Therefore, antacid therapy should be used in low doses and very cautiously, with routine monitoring of serum calcium and phosphorus in children taking medications which reduce gastrointestinal phosphate absorption.

Background: It is generally accepted that functional dyspepsia is caused by heterogeneous pathogenetic factors. From the clinical point of view acid-related symptoms as heartburn, acid regurgitation and epigastric pain (acid-type) can be separated from general dyspeptic symptoms as predominant fullness, nausea/vomiting (dysmotility-type)., Patients and Methods: In the present study, the influence of a four-week-treatment with ranitidine (twice 150/d, n = 346) in comparison with an antacid (40 mmol/d, n = 340) on the severity and course of symptoms in patients suffering from an acid-related functional dyspepsia was investigated., Results: With ranitidine, acid-related as well as general dyspeptic symptoms disappeared in a significantly higher percentage after two and four weeks compared with antacid. Complete disappearance of symptoms was documented with ranitidine after two weeks in 37% and after four weeks in 66% compared with antacid in 13% and 30% respectively (p < 0.005). Patients with severe symptoms, history of ulcer and long-term dyspepsia and slight endoscopic changes in the upper gastrointestinal tract showed a significant faster and more distinct response. Both kinds of treatment were well tolerated., Conclusion: It is concluded that in acid-related functional dyspepsia ranitidine is superior to antacid in relieving symptoms. Therefore, a probative treatment with ranitidine up to four weeks is recommended as a practical therapeutic alternative in this syndrome.

We retrospectively investigated the efficacy of high dose omeprazole compared to a combined therapy of famotidine, pirenzepine and antacid for acute upper gastrointestinal hemorrhage (AUGIH) also adjuvant to endoscopic injection therapy if indicated. The clinical course of AUGIH was evaluated, if emergency endoscopy revealed lesions substantially dependent on intragastric acidity with respect to pathogenesis and/or healing (peptic ulcer, erosive gastroduodenitis, reflux-esophagitis, Mallory-Weiss tears) and patients either received a combined therapy of famotidine (20 mg i.v. every 12 hrs), pirenzepine (10 mg i.v. every 12 hrs) and antacid (control group: n = 96) or omeprazole (40 mg i.v. every 6 hrs; omeprazole group: n = 100). Rate of rebleeding was lower in the omeprazole group without reaching significance (12 vs. 21; p = 0.06). No difference was found for rates of operation (6 vs. 6; p = 0.94), death from bleeding (5 vs. 9; p = 0.22), transfusions ([mean +/- SD] 3.3 +/- 5.0 vs. 3.2 +/- 5.7; p = 0.51) and hospitalisation ([mean +/- SD] 26.8 +/- 12.1 vs. 27.8 +/- 16.0 days; p = 0.88). Considering prognostic risk factors (age > or = 65, actively bleeding lesion, initial state of shock) logistic regression showed that high dose omeprazole inhibited rebleeding (p = 0.01) but had no effect as regards surgery or mortality. Within two selected subgroups defined by additional criteria (no endoscopic treatment and anamnestic peptic lesion) omeprazole-treated cases showed lower rates of rebleeding (3/49 vs. 12/54, p " 0.02 and 3/44 vs. 13/48, p = 0.01 resp.) and death from bleeding (0/46 vs. 6/50, p = 0.03 and 0/43 vs. 5/45, p = 0.03 resp.).(ABSTRACT TRUNCATED AT 250 WORDS)

Basic modes of action and indications for aluminium and magnesium-containing antacids are reviewed. Antacid properties of Maalox were studied versus those of Almagel in 24 duodenal ulcer patients by the following indices of pH-metry: time of pH response onset, "alkaline time", alkalification area and index. All the features were significantly different when assessed in the body of the stomach. Regular Maalox intake as a main medicine provided good results in the treatment of duodenal ulcer (25 responders), gastric ulcer (14 responders), erosive gastroduodenitis (14 responders), erosive reflux-esophagitis (9 responders). Maalox displayed high symptomatic efficacy, safety, insignificant side effects.

Objective: To determine the occurrence of upper gastrointestinal hemorrhage in critically ill children, and the efficacy of prophylaxis with almagate (antacid), ranitidine, and sucralfate., Design: Prospective, randomized, controlled trial., Setting: Pediatric ICU of a tertiary care pediatric hospital., Patients: During a 2-yr study period, 165 patients with one or more upper gastrointestinal hemorrhage risk factors were randomized into one of four groups. Twenty-five patients were excluded because of protocol violations. A total of 140 patients completed the study, with 35 patients in each group., Interventions: Patients received no treatment in the control group. The antacid group received almagate 0.25 to 0.5 mL/kg every 2 hrs by nasogastric tube. The ranitidine group received 1.5 mg/kg every 6 hrs iv. The sucralfate group received 0.5 to 1 g every 6 hrs by nasogastric tube., Methods: Gastric pH and macroscopic bleeding were determined every 2 hrs in all patients until the end of the study. Macroscopic bleeding was classified as nonhemorrhage, slight, or important. Microscopic gastric bleeding was researched with guaiac testing in 72 patients (680 samples). The severity of illness was evaluated by using the Therapeutic Intervention Scoring System, Physiologic Stability Index, and the Multiorgan System Failure scores. The risk of upper gastrointestinal hemorrhage was evaluated by the Zinner and Tryba indices, and was modified for children., Measurements and Main Results: The occurrence rate of important upper gastrointestinal hemorrhage was higher (by 20%) in the control group than in the rest of the groups (5.7%), p less than .01. There were no differences between the other groups (almagate 5.7%, ranitidine 8.5%, and sucralfate 2.8%). There was a statistically significant correlation between the occurrence rate of important upper gastrointestinal hemorrhage, the scores of severity of illness indices (Therapeutic Intervention Scoring System, Physiologic Stability Index, and the Multiorgan System Failure scoring system), the risk of upper gastrointestinal hemorrhage indices (Zinner and Tryba), and mortality rate. The Zinner index better classified the patients in relation to the onset of important upper gastrointestinal hemorrhage (sensitivity 76.9%, specificity 85.8%)., Conclusions: Upper gastrointestinal hemorrhage is an important complication in critically ill children. Prophylaxis with almagate, ranitidine, or sucralfate reduces the occurrence rate of clinically important gastrointestinal hemorrhage.

Antacid (AA) in a very low dose (88 mmol/day) was compared to the standard 800-mg dose of cimetidine in healing duodenal ulcers. The influence of sex, age, symptom duration at entry, night pain, smoking, coffee consumption, and alcohol on ulcer healing was studied. The antacid was given in two different schedules: group I--20 ml 1 hr after breakfast and at bedtime; group II--10 ml 1 hr after breakfast and lunch and 20 ml at bedtime. Cimetidine (group III) was given in two divided doses: 400 mg 1 hr after breakfast and 400 mg at bedtime. Endoscopic control was performed after four weeks and, if necessary, after eight weeks of treatment. The healing rate after four weeks of treatment was, respectively, for groups I, II, and III, 45.5%, 55.8%, and 69.4% (group I = group II, and group III different from groups I and II). After eight weeks of treatment the healing rate was 61.5%, 80.8%, and 88.0% for groups I, II, and III, respectively (group II = group III, and group I different from groups II and III). Except for group I, smoking did not influence healing rate. Age, sex, symptoms at entry, night pain, and coffee consumption did not influence the treatment results. The authors concluded that the very low dose of magaldrate (88 mmol/day), when administered in three divided doses (10 ml after breakfast and lunch and 20 ml at bedtime) for eight weeks was as effective as 800 mg of cimetidine (400 mg twice a day) in healing duodenal ulcer.

The efficacy of ranitidine 150 mg twice daily and Maalox TC three tablets four times daily were compared in patients with endoscopically confirmed duodenal ulcer. Seventy-nine patients were randomly allocated to double-blind, double-dummy treatment, stratified for smokers. Endoscopy was repeated after four weeks. Those unhealed continued treatment for a further two weeks before final endoscopy. Per protocol analysis in 53 patients showed ulcer healing rates at week 4 and at weeks 4 and 6 combined of 78 and 89% on Maalox TC, and of 81 and 91% on ranitidine, respectively. The same analysis gave overall healing rates of 81% in smokers and 100% in nonsmokers, irrespective of treatment. Both treatments provided early ulcer pain relief. Diarrhea was a commoner side effect in patients on Maalox TC. The study showed Maalox TC and ranitidine were equally effective in healing duodenal ulceration.

Background: There is no specific method of diagnosing magnesium-induced diarrhea. Therefore, the frequency and clinical importance of diarrhea caused by magnesium are unknown. The purposes of this study were to establish a method for diagnosing magnesium-induced diarrhea and to apply it to patients with chronic diarrhea., Methods: We measured fecal output of soluble magnesium and fecal magnesium concentration in 19 normal subjects with formed stools (15 collection periods), with non-magnesium-induced diarrhea (36 collection periods), and with diarrhea induced by magnesium hydroxide alone (11 collection periods) or in combination with phenolphthalein (3 collection periods), and in 359 patients with chronic diarrhea., Results: The upper limits of fecal output of soluble magnesium and fecal magnesium concentration in normal subjects were 14.6 mmol per day and 45.2 mmol per liter, respectively. When normal subjects had diarrhea due to the ingestion of magnesium hydroxide alone or in combination with phenolphthalein, fecal magnesium output was always abnormally high. For each millimole increase in fecal magnesium output, fecal weight increased by approximately 7.3 g. The fecal magnesium concentration was very high when magnesium was the only cause of diarrhea but only moderately elevated when diarrhea was induced by magnesium hydroxide plus phenolphthalein. Biochemical and clinical evidence indicated that excessive ingestion of magnesium was an important cause of chronic diarrhea in 15 of the 359 patients with chronic diarrhea (4.2 percent), if not the only cause., Conclusions: Quantitative fecal analysis for soluble magnesium is an accurate method of diagnosing magnesium-induced diarrhea. Some patients with chronic diarrhea ingest excessive amounts of magnesium (in antacids or food supplements), and physicians may fail to discover this before embarking on an expensive and invasive diagnostic evaluation.

1. The effect of magnesium hydroxide on the oral absorption of ibuprofen, ketoprofen and diclofenac was investigated in two randomized cross-over studies, both consisting of two phases. 2. Single doses of magnesium hydroxide (850 mg) or of water (150 ml) only were given to six healthy volunteers immediately after the ingestion of ibuprofen (400 mg, Study 1), ketoprofen (50 mg, Study 2) or diclofenac (50 mg, Study 2). Plasma drug concentrations were measured up to 24 h. 3. Magnesium hydroxide increased the area under the plasma ibuprofen concentration-time curve between 0 and 1 h by 65% (P less than 0.05) and the peak concentration of ibuprofen in plasma by 31% (P less than 0.01). The time to peak was shortened by about 0.5 h. The extent of bioavailability of ibuprofen was not increased by magnesium hydroxide. 4. Neither the rate nor the extent of absorption of ketoprofen or diclofenac was changed significantly by magnesium hydroxide. 5. When rapid onset of the analgesic effect of ibuprofen is required, concomitant ingestion of an antacid, which contains magnesium hydroxide without aluminium, is recommended.

We present what we believe is the first case of rickets following prolonged treatment with aluminum containing antacids that bind phosphate, in an 18-year-old mentally retarded boy with cerebral palsy and spastic quadriplegia. As expected, serum calcitriol was increased and urinary phosphate excretion was very low. However, in contrast to all published cases of antacid induced hypophosphatemic osteomalacia in adults, despite a substantial increase in bone resorption reflected by urinary total hydroxyproline excretion, urinary calcium excretion was low rather than high, and significant hypocalcemia occurred after antacids were ceased and a phosphate salt administered. We suggest that the skeleton was so under-mineralized because of growth during prolonged phosphate deficiency, possibly augmented by anticonvulsant administration and immobilization, that increased bone resorption did not release enough calcium to cause hypercalciuria, or to prevent hypocalcemia during resumption of normal mineralization.

A 42-year-old woman presented to our institution with a 2-week history of bone pain in the lower extremities. Her history was remarkable for duodenal ulcer and long-term treatment with a magnesium-aluminum hydroxide antacid (Maalox) and sucralfate. Initial laboratory studies showed severe hypophosphatemia and elevated alkaline phosphatase and serum 1,25-dihydroxyvitamin D levels. Bone scan showed multiple areas of increased uptake consistent with osteomalacia and microfractures. The patient recovered completely following withdrawal of antacids and sucralfate and short-term treatment with phosphate. Although hypophosphatemia induced by aluminum-containing antacids is rare, treatment of peptic ulcer disease with a combination of two aluminum-containing agents may increase the risk of clinically significant hypophosphatemia. Awareness of this condition is important, because early recognition can prevent morbidity and lead to safe and effective treatment.

Two cows, 1 with diarrhea and 1 with signs of forestomach outflow obstruction, were treated in part with repeated doses of a commercially available antacid/cathartic preparation containing magnesium hydroxide. Both cows subsequently were determined to have hypermagnesemia, along with severe metabolic alkalosis. In addition, each cow was comatose at the time of death. A clinical study was initiated to investigate the causal relationship between the ingestion of magnesium hydroxide and the generation of hypermagnesemia and metabolic alkalosis in adult cows. Twelve healthy mature cross bred beef cows were allotted at random to a fed or fasted (simulated anorexia) group, with 2 untreated and 4 treated cows in each group. A single dose of magnesium hydroxide (1.5 g/kg of body weight, suspended in 3.8 L of warm water) was administered per os to each treated cow, whereas each control cow was given only water. Individual determinations of selected venous blood gas values (plasma bicarbonate ion [HCO3-] concentration, and base excess [BE]), serum magnesium (Mg) concentration, and urine magnesium fractional clearance ratio (Mg-FCR) were made immediately before drug administration, and at 2, 4, 8, 12, 24, and 36 hours after treatment. Compared with control values at the conclusion of the study, mean serum Mg concentration, urine Mg-FCR, plasma HCO3- concentration, and BE were significantly higher (P = 0.0001, P = 0.0015, P = 0.028, and P = 0.021, respectively) in treated cows.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of aspiration of (a) 2 ml of Mylanta (a particulate antacid) mixed with 2 ml of hydrochloric acid (pH 1.5), (b) 2 ml of half-strength Bicitra (a soluble antacid) mixed with 2 ml of hydrochloric acid (pH 1.5), (c) 4 ml of hydrochloric acid (pH 1.5), and (d) 4 ml of normal saline (pH 6.5) on arterial blood gas tensions and lung pathology were compared in anesthetized rabbits. PaO2 decreased similarly in all animals 15 minutes after aspiration, but recovered to normal levels 4 hours after aspiration of saline and 48 hours after aspiration of Bicitra. PaO2 remained depressed after aspiration of Mylanta and HCl. Gross and microscopic evidence of lung injury was most severe in animals that aspirated Mylanta. One animal died 8 hours after aspiration of Mylanta.

A 69 year old man presented with painful proximal muscle weakness which clinically simulated polymyositis. Further evaluation revealed normal muscle enzymes and hypophosphatemia which resulted from unsuspected antacid abuse. "Pseudo-myopathy" is one example of the myriad of rheumatic diseases which may be mimicked by hypophosphatemia.

A randomized, prospective, crossing-over clinico-pharmacological study was conducted on the tolerability by humans, of TISACID (Al-Mg-hydroxy-carbonate), a new antacid of up-to-date composition produced in Hungary. Even a relatively high dose of the preparation is tolerated by the human organism. During a 6-week continuous treatment neither subjective nor objective side-effects were observed. The tablet is immediately decomposed in the gastric juice, a considerable portion of it will permanently stick to the mucosa of the stomach and duodenum. Depending on the dose, it rapidly and permanently reduces the acidity of the gastric content and increases serum gastrin concentration only moderately and for a short time. Administered together with cimetidine, it promotes healing of duodenal ulcer and the cessation of complaints. It does not increase the aluminium and magnesium concentrations of the plasma not even on prolonged administration, and clinical symptoms and laboratory changes characterizing the phosphate depletion syndrome do not develop either. Based on the results, authors consider Tisacid a beneficial preparation as regards both effectivity and tolerability.

To control hyperphosphataemia without hyperaluminaemia, A1(OH)3, which was given in addition to high doses of oral calcium, was replaced by Mg(OH)2 for 6 months in 20 haemodialysed patients and for 20 months in 12. The treatment during the control period was 110 +/- 91 mmol/day of oral calcium element given as CaCO3 and/or Calcium Sorbisterit and 1.05 +/- 1.47 g/day of A1(OH)3. Haemodialysis treatment was 4 h, thrice weekly. To prevent hypermagnesaemia, dialysate magnesium was decreased from 0.75 mmol/l to 0.375 mmol/l. After a control period of 3 months, Mg(OH)2 was given at a mean dose of 2.6 +/- 2 g/day and oral calcium supplements were decreased to 76 mmol/day. Two subsequent bone histomorphometry studies were performed at 8 month intervals in four patients and at 20 month intervals in seven patients. The results show a good control of plasma calcium (mean +/- SD: 2.43 +/- 0.1 mumol/l); phosphate (1.76 +/- 0.4 to 1.66 +/- 0.3 mmol/l); aluminum (1.3 +/- 0.1 mumol/l to 0.6 +/- 0.1 mumol/l); alkaline phosphatase (135 +/- 65 to 125 +/- 40 IU); and PTH fragments (PTH C terminal decreased from 260 +/- 214 to 185 +/- 182 pg/ml, PTH medium from 4185 +/- 5113 to 2270 +/- 4880 pg/ml). Plasma magnesium increased from 0.96 +/- 0.2 to 1.54 +/- 0.2 mmol/l. Bone histomorphometry shows no change in mineralisation, and a borderline decrease of resorption parameters. The main side-effects are (1) diarrhoea, which was well controlled by transient treatment with karaya gum, and (2) an increased need for potassium binders.(ABSTRACT TRUNCATED AT 250 WORDS)

The effectiveness of antacid maintenance therapy in preventing duodenal ulcer (DU) relapse was investigated. Two hundred and fifty one asymptomatic patients with healed DU were stratified into smokers and non-smokers and randomised to receive for one year either placebo, or Maalox TC three tablets (81 mmol) at bedtime (hs), or Maalox TC three tablets in the morning plus three tablets at bedtime (bd) (162 mmol), or cimetidine 400 mg at bedtime. A double dummy technique was used to render the study double blind. In 176 patients evaluable for efficacy, the cumulative relapse at one year was: placebo 57%; Maalox TC hs 39%; Maalox TC bd 23%; cimetidine 25%. Maalox TC bd and cimetidine were equally effective and superior to placebo (p less than 0.01) and bedtime Maalox TC (p less than 0.04). The benefit of treatment was significant for the overall sample and for the subgroup of smokers. The results for the non-smokers also supported efficacy for these two treatments but, perhaps because of small sample sizes, these comparisons were not significant. All 251 patients were assessed for safety. Approximately half the patients in each treatment group had adverse events, leading to withdrawal in three, seven, 12, and four patients on placebo, Maalox hs, Maalox bd, and cimetidine respectively. Diarrhoea occurred in 12 patients in Maalox TC bd and eight in each other group. Serum magnesium concentrations were unchanged; aluminium concentrations were higher than baseline at six and 12 months in both antacid groups and at 12 months in the cimetidine group but the differences were not significant. Maalox TC three tablets bd are as effective as cimetidine 400 mg at bedtime in reducing DU relapse and both are superior to placebo.

In an open safety-in-use study, the subjective effectiveness and taste acceptability of a new high-potency antacid product were compared to previous treatment in 109 patients presenting with upper gastro-intestinal disorders of functional origin. Severity of the dominant symptoms prior to treatment was compared with that of symptoms present during treatment. Sixty-seven per cent to 73% of upper gastro-intestinal tract symptoms were completely relieved. Eighty-three per cent versus 48% of patients seen in a private practice setting, as compared with the speciality practice, reported good to excellent results, with 92% versus 56% describing good to excellent taste acceptability. When compared with previous antacid therapy, 70% of the patients preferred the new high-potency formulation to the regular-strength products, for both effectiveness and taste. The incidence of product-related side-effects was low, with only 6.7% experiencing the diarrhoea or loose stools commonly associated with conventional products containing magnesium hydroxide.

Fifty consecutive patients with symptomatic endoscopically proven duodenal ulcer were randomized double-blind to Mylanta II or cimetidine treatment schedules. Smoking habits were noted, but patients were not advised to alter these. Healing was determined by reendoscopy at 6 wk. Eighty percent of patients on active cimetidine and 52% on active Mylanta II had healed at 6 wk (not significantly); 85% of nonsmokers healed compared to 44% of smokers (p less than 0.03). In smokers, cimetidine achieved healing in 50%, Mylanta II in 39% (not significantly); while in nonsmokers, cimetidine achieved healing in 100%, Mylanta II in 67% (not significantly). These results indicate a significant and equally adverse effect of smoking on the healing rate of duodenal ulcer achieved by either cimetidine or Mylanta II.

A 63-year-old man had an acute small bowel obstruction while being treated with ranitidine and self-prescribed antacid. On exploration, a firm mass, chemically similar to the ingested antacid, was found impacted in the terminal ileum. We believe the effect of ranitidine on gastric secretory volume was the cause of the antacid concretion.

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.

One hundred twenty-six parturients for elective cesarean section under general anesthesia were allocated to either a cimetidine or an antacid group in a randomized, double-blind, multicenter trial. The cimetidine-treated group received 300 mg cimetidine orally the evening before the operation and 300 mg intramuscularly between 1 and 3 h preoperatively. The antacid-treated group received 30 ml of Mylanta-II orally on both occasions. Gastric volume, 30 min after induction of anesthesia and 30 min before response to oral commands, was less in the cimetidine-treated group. Gastric pH 30 min after induction was greater in the cimetidine-treated group. The maternal serum level of cimetidine at birth was 1.31 +/- 0.12 micrograms/ml and the umbilical venous level was 0.78 +/- 0.05 micrograms/ml. The neonatal gastric acidity, Apgar scores, and Early Neonatal Neurobehavioral Scale (ENNS) scores were similar in both groups. No maternal or neonatal complication was attributed to treatment.

TISACID (a new, modern Hungarian Al-containing antacid) with a high acid-neutralizing capacity (greater than 26.8 mmol/g) also enhances gastric mucosal defense mechanisms (prostaglandin-dependent gastroprotection). A simple-blind, prospective, randomized, parallel multicentre clinical trial has been performed on both the clinical efficacy and possible side effects of TISACID monotherapy (Al-Mg-hydroxy-carbonate) on informed patients suffering from active duodenal ulcers. The study groups were as follows: Group "A": 3 g/day of TISACID (acid-neutralizing capacity = 78 mmol, n = 85), Group "B": 6 g/day of TISACID (acid-neutralizing capacity = 156 mmol, n = 88), Group "C": 12 g/day of TISACID (acid-neutralizing capacity = 312 mmol, n = 68), Group "D": (as control): (1.0 g/day cimetidine (HISTODIL, RGH, Budapest, n = 91). The total number of patients: 332. It was found that: 1. The new Hungarian antacid compound (both tablet and suspension) can essentially accelerate the healing rate of duodenal ulcers. 2. The cumulative healing rate of ulcers and the decrease of complaints can be achieved equally by relatively low doses of TISACID monotherapy and cimetidine alone. 3. There were no differences between the clinical potency and side-effects of TISACID tablet and suspension.