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In our recent study, oral cimetidine increased carbamazepine plasma levels after a single oral dose by 26 percent and prolonged the elimination half-life by 18 percent. This effect of cimetidine on carbamazepine could have resulted from enhanced carbamazepine absorption and/or inhibited metabolism. To gain an insight into which mechanism was responsible, we repeated the study with ranitidine, which has nearly identical gastrointestinal effects as cimetidine, but does not inhibit oxidative metabolism. Eight healthy subjects received a single dose of carbamazepine 600 mg po on two occasions separated by one month. In a randomized sequence, they also received ranitidine 300 mg/d or matching placebo starting two days before and continuing until seven days after the carbamazepine dose. Ranitidine did not change the carbamazepine area under the plasma concentration-time curve (324.2 +/- 71.1 micrograms h/ml, placebo vs. 326.3 +/- 65.0 micrograms h/ml, ranitidine; p = 0.84) or the elimination half-life (32.2 +/- 6.4 h, placebo vs. 31.7 +/- 6.1 h, ranitidine; p = 0.62). Since ranitidine does not alter the pharmacokinetic profile of oral carbamazepine, it is unlikely that the changes observed with cimetidine were due to increased carbamazepine absorption. Therefore, the mechanism of the single-dose carbamazepine-cimetidine interaction is probably metabolic inhibition, although the exact pathway (or pathways) affected has not been identified.
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The efficacy and safety of famotidine and ranitidine in the treatment of active duodenal ulcer were compared in a multicenter, randomized double-blind study. The study was carried out in 5 centers which included a total of 143 patients with endoscopically documented active duodenal ulcer. The patients received either famotidine (1 tablet of 40 mg at night) or ranitidine (2 tablets of 150 mg at night). Endoscopic examinations were performed at 4 and 6 weeks of active treatment. Day and nocturnal pain were also monitored and the laboratory and clinical profiles evaluated. One hundred and thirty-three patients fulfilled the evaluation criteria (66 patients in the famotidine group and 67 in the ranitidine group). Healing rates at weeks 4 or 6 of treatment showed no significant differences between the famotidine and the ranitidine groups. The healing rates were 79% at week 4 and 96% at week 6 in the famotidine group, and 77% at week 4 and 95% at week 6 in the ranitidine group. Similar results were observed in both treatment groups with regard to pain resolution, decrease in antacid intake and safety profile.
Ranitidine is a generally well-tolerated drug, and serious side effects are rare. However, ranitidine-induced anaphylaxis has been reported on rare occasions. We report on such a case and review other cases reported in the literature.
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A double-blind clinical investigation was conducted to study the effectiveness of ranitidine therapy in 52 patients with gastritis that had been confirmed by panendoscopy. Subjective weekly assessment of symptoms showed that patients receiving 300 mg of ranitidine daily for four weeks improved considerably more than those receiving placebo. In the ranitidine-treated group, symptoms completely disappeared in 20 (80%) of 25 patients and significantly improved in the other five; in the placebo group, only nine (45%) of 20 patients improved, with the remaining 11 staying unchanged (seven patients--one in the ranitidine-treated group and six in the placebo-treated group--did not return to the hospital and so were withdrawn from the study). Panendoscopy repeated in 41 patients at the end of the four-week treatment period confirmed the assessment of symptoms. No significant adverse effects were observed in patients taking ranitidine. This investigation found ranitidine to be an effective short-term treatment for patients with endoscopically proved gastritis.
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Ranitidine clearance by hemodialysis is significantly higher with PS than with CP. Although additional dose adjustment may not be needed for ranitidine, the type of dialyzer membrane can affect drug elimination and should be taken into account for consideration of drug removal by hemodialysis.
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There is obvious advantage in treating peptic ulcers by the combination of Jianweiyuyang granules and ranitidine capsules, and its mechanisms may be to protect the gastric mucosal barrier by up-regulating the expression of MUCSAC mRNA and to improve the gastric mucosal blood flow by down-regulating the expression of ETAR mRNA.
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1. Twelve healthy men drank 0.80 g ethanol kg-1 body weight on four occasions spread over several weeks. Ethanol was given as 96% v/v solvent which was diluted with orange juice to make a cocktail (20-25% v/v). This drink was ingested in exactly 30 min at 08.00 h after an overnight (10 h) fast. 2. Samples of venous blood were obtained at exactly timed intervals of 0, 10, 20, 30, 45, 60, 90, 120, 150, 180, 240, 300, and 360 min after the start of drinking. The concentrations of ethanol in whole blood were determined by headspace gas chromatography. 3. Summary measures were used to evaluate the concentration-time profiles of ethanol for each subject. The between-subject and within-subject components of variation for the pharmacokinetics of ethanol were derived by one-way analysis of variance (ANOVA). 4. The variation between different subjects dominated the total variance for all of the pharmacokinetic parameters studied except the rate of disappearance of ethanol from blood (ko). For this latter parameter, 42% and 58% of the total variation arose from variations between- and within-subjects respectively. These results might be important to consider when experiments on the clinical pharmacokinetics of ethanol are being planned.
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To study two groups of patients intubated with different prophylaxis of stress gastric ulcer in a prospective randomized trial. The differential effect on gastric pH, gastric colonization and the incidence of pneumonia associated to mechanical ventilation (PMV) were analyzed.
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1. The effects of single daily doses of 20, 50 and 150 mg of WY-45,727, a novel H2-receptor antagonist, and placebo were compared using long term pH-monitoring in 20 male volunteers. 2. Intragastric acidity was measured using combined Ingold glass electrodes. Subjects underwent four studies each under identical dietary conditions. Medication was taken after the evening meal. 3. Median 24 h pH rose from 1.3 (1.2-1.4 interquartile range) on placebo to 1.9 (1.6-2.8) on 20 mg WY-45,727, to 3.1 (2.3-3.7) on 50 mg WY-45,727 and to 4.5 (3.7-4.7) on 150 mg WY-45,727. All three doses increased 24 h and night-time pH significantly compared with placebo (P less than 0.0001). 4. The PAGE test for order effects confirmed clear dose dependent inhibition of acidity (P less than 0.0001). 5. Highly consistent individual responses were found during the night following 150 mg WY-45,727.
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To compare the efficacy of omeprazole, a proton pump inhibitor, with Histamine H2 receptors antagonists in the control and recurrence of non-variceal upper gastrointestinal bleeding.
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Antiulcer activity of Andrographis paniculata was evaluated by cysteamine induced duodenal ulcer model in rats. Male albino Wistar rats were pre-administered with 200 mg/kg body wt. of hydroalcoholic extact of Andrographis paniculata (HAEAP) orally, for 30 days prior to i.p. administration of 420 mg/kg body wt. of cysteamine as a single dose. Rats preadministered with 30 mg/kg body wt. of ranitidine served as standard drug. Ulcer index, thiobarbituric acid reactive substances, mucin, glutathione peroxidase and myeloperoxidase activities, reduced glutathione/oxidized glutathione (GSH/GSSG) ratio, glycoproteins and membrane bound enzyme activities were measured in duodenum of experimental animals. The ulcer score and myeloperoxidase activity were significantly minimized in rats treated with HAEAP. Mucin content was found to be preserved in rats treated with the extract. GSH/GSSG ratio and glutathione peroxidase activities were found to be maintained by the HAEAP. Level of lipid peroxidation products was found to be significantly low in HAEAP treated rats compared to ulcer control rats. The basolateral and brush border membrane bound enzyme activities which were depleted significantly in ulcer control rats were found to be maintained in rats pre-treated with the extract. The ulcer preventing effect was comparable to that of ranitidine treated rats. Level of glycoproteins was also found to be preserved in rats treated with the extract. The normal rats treated with the HAEAP did not show any abnormal alterations in the parameters studied. Histopathological observations also showed the ulcer preventing effect of the HAEAP. It is suggested that the ulcer preventing effect may be due to its mucin preserving and antioxidant nature.
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Transient ischemia was produced for 15 min by occlusion of the middle cerebral artery in halothane-anesthetized rats, and changes in the extracellular concentrations of neurotransmitter monoamines and amino acids were examined in the striatum. The occlusion produced marked increases in the extracellular concentrations of both dopamine and glutamate in the striatum in the saline-injected control group, the peak values being 148 and 5.2 times those before ischemia, respectively. Preischemic administration of histamine (200 nmol, i.c.v.) suppressed the increase in dopamine and glutamate levels during ischemia, the peak values being 38% and 40% of those in the control group, respectively. Neither the dopamine nor glutamate level was affected by 6-[2-(4-imidazolyl)ethylamino]-N-(trifluoromethylphenyl)heptanecarboxamide (HTMT), an H(1) agonist (100 nmol, i.c.v.). However, dimaprit, an H(2) agonist (100 nmol, i.c.v.) suppressed the peak values to 42% and 32%, respectively. Most neurons were degenerated 7 days after ischemia in control animals. Histologic outcome was alleviated by either histamine or dimaprit treatment, whereas HTMT did not affect the outcome. Although postischemic administration of mepyramine, an H(1) antagonist (5 nmol, i.c.v.), did not affect the histologic alleviation caused by preischemic treatment with histamine, ranitidine, an H(2) antagonist (30 nmol, i.c.v.), partly abolished the improvement caused by histamine. These results suggest that suppression of ischemic release of excitatory neurotransmitters by histamine H(2) action is a contributing factor in alleviation of histologic outcome.
Histopathologically the glucocorticoid group showed wide medullary cavities with wide osteocytic lacunae. These marrow cavities were reduced in the prophylactic groups (III, IV) but increased in group V. Bone histomorphometric analysis revealed improvement in static bone parameters in groups III and IV and deterioration in group V in comparison to group II. The DEXA revealed significant reduction in the bone mineral density in all experimental groups compared to the control group.
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Using a randomized 4-way cross-over design, cats were given enteric-coated omeprazole granules (1.1-1.3 mg/kg q24h and q12h), ranitidine (1.5-2.3 mg/kg q12h), and placebo. Intragastric pH was monitored continuously for 96 hours using the Bravo(™) system, starting on day 4 of treatment, followed by a median washout period of 12 days. Mean percentage of time pH was ≥3 and ≥4 was compared among groups using repeated measures ANOVA.
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H. pylori was cultured and clarithromycin susceptibility was determined before and after treatment, from duodenal ulcer patients receiving RBC and clarithromycin or omeprazole and clarithromycin for 2 weeks in a multicenter randomized clinical trial.
The focus was on haloperidol (central dopamine antagonist)-stomach lesion, a longly described suitable counterpart of dopamine blocker cysteamine-duodenal lesion. In this, the contribution of blockade of central/peripheral dopamine receptors and prostaglandins synthesis, along with influence of antiulcer agents was evaluated in mice. Male NMRI Hannnover mice were sacrificed 24 h after haloperidol (25 mg/kg b.w. i.p., given alone or with saline (haloperidol+saline) (i) or in combination (ii,iii)). Supporting central dopamine predominance for haloperidol stomach lesion induction, co-administration of peripheral dopamine receptor antagonist domperidone (5 mg/kg i.p.) (haloperidol+ domperidone) (ii), or prostaglandin synthesis inhibitor indomethacin (10 mg/kg s.c.) (haloperidol+ indomethacin) (iii) did not aggravate this lesion. (i) In haloperidol+saline challenged mice the lesions were inhibited by co-administration (/kg i.p.) of a gastric pentadecapeptide BPC 157, GlyGluProProProGlyLysProAlaAspAspAlaGlyLeuVal, M.W. 1419 (10 microg, 10 ng, 10 pg, but not 1 pg, 100 fg, 10 fg), bromocriptine (10 mg), omeprazole (10 mg, 100 mg, but not 1 mg). Atropine (10, 100, 200 mg), pirenzepine (10, 100, 200 mg), misoprostol (10, 100, 200 microg), pantoprazole (1, 10, 100 mg), lansoprazole (0.1, 1, 10 mg), cimetidine (10, 100, 200 mg) and ranitidine (10, 100, 200 mg) were not effective. (ii) Dopamine peripheral blockade influence: in haloperidol+domperidone mice, previously effective bromocriptine, pentadecapeptide BPC 157 (10 microg) or omeprazole (10 mg) did not attenuate stomach lesions. (iii) Prostaglandins synthesis blockade effect: in haloperidol+indomethacin mice, previously effective agents, bromocriptine or omeprazole were not active, while BPC 157 effect was only lessened.
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To verify if cimetidine, ranitidine, and famotidine, when inoculated by ip route in mice, do enhance macrophage activation and whether or not such activation is altered with prior use of sodium thioglycolate. KIND OF STUDY: Experimental.
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The pathophysiology of stress ulcers is complex. There is either too much acid and pepsin or inadequate mucosal defenses. The incidence of upper GI bleeding due to stress ulcers in the ICU is 5-25% depending upon the minimum criterion of bleeding. For the individual patient the risk of bleeding is determined by his underlying condition and the number of risk factors. SAPS and APACHE II may assist in identifying those patients. Attainment of an increase in intragastric pH is effective and frequently necessary to prevent stress ulcer bleeding and reduces the incidence of overt bleeding. Based on presently available information the most suitable regime for prevention of stress ulcer bleeding is a continuous infusion or fixed bolus dosing of cimetidine or ranitidine. With respect to the side effects, ranitidine appears to be the more favorable of these two H2 blockers. The position of sucralfate in the prophylaxis has not yet been established.
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Although gastric acidity is essential for the development of DU, the pathogenesis is more complex and includes an imbalance in the "defending" forces, mainly in mucous secretion, prostaglandin and bicarbonate synthesis and cell turnover. The new drugs available for inhibition of acid secretion, ulcer isolation and cytoprotection make it possible to attack the problem from different sites. The decision of which drug to choose should take into account side effects, drug interactions, cost and recurrence.
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One hundred and twenty patients were randomly divided into 6 groups. Another 10 patients as the control group were confirmed with no peptic ulcers by endoscope, but had digestive tract symptoms. The clinical effects were compared among each group after the one month treatment.
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Intravenous cimetidine, 300 mg or 400 mg, or ranitidine, 50 mg, was administered as a single dose to 36 volunteers in a randomized, crossover fashion. Aspirates of gastric juice were obtained after dosing, and the pH, titratable acidity, gastric fluid volume, and gastric acid output were determined from baseline through 71/2 hours for each subject. Each intervention significantly increased pH and suppressed hydrogen ion concentration, gastric fluid volume, and gastric acid output. Both the magnitudes of the changes when compared with baseline and the time of the mean maximum effects were similar in all three drug regimens. The effect of all three interventions on gastric fluid volume and gastric acid output diminished sharply after 6 hours. The data indicate that the gastric secretory response to all three interventions did not differ substantially.
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PVC matrix membrane selective electrodes for ranitidine, nizatidine and famotidine, based on sparingly soluble complexes, were prepared and characterized. The optimum functional pH range, response time, selectivity and lifetime were determined for each of the built electrodes. The linear range, precision and accuracy of each method were obtained by statistical interpretation of experimental results, while the limit of detection and thelimit of quantification were determined by a graphical method. All these electrodes were applied for the direct quantitative potentiometric determination of ranitidine hydrochloride, nizatidine and famotidine in pharmaceutical formulations.
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No implications for practice at this stage can be concluded. Appropriately designed large-scale randomized controlled trials with long-term follow up are needed to determine the effects of additional bedtime H(2)RAs in suppressing NAB.
H2R-ANT adjunctive therapy did not improve overall symptoms. To clarify the opposite results between body weight and BMI, future research should investigate long-term efficacy and generate more safety data by using larger samples.
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Problems after Helicobacter pylori (Hp) eradication therapy include recurrence of Hp-negative peptic ulcers. We investigated the pathophysiological characteristics of Hp-negative recurrent ulcer scars, and performed proton pump inhibitor (PPI) maintenance therapy as a new therapy for prevention of recurrence in patients with Hp-negative recurrence after Hp eradication and investigated its usefulness.
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This paper reports the results of a multicenter prospective study of 188 consecutive patients affected by gastric ulcer, verified by endoscopy, in whom the frequency of a mycotic infection of the lesion was evaluated as well as the eventual influence of such pathology on the efficiency of medical treatment, the healing rate, and the healing time. A mycotic infection, defined as penetration of the periulcerous mucosa by the fungi, was found in only 13 patients (6.9%). No significant differences were found in the healing rate and healing time among these patients treated with H2-receptor antagonists and a control group of 43 matched gastric ulcer patients treated in the same period with the same therapy. It would appear from the data that mycotic infections of the gastric ulcer do not modify the efficiency of medical treatment.